bluuebunny/crossref_metadata_2025 huggingface dataset:
Hemorrhage effects on plasma ANP, NH2-terminal pro-ANP, and pressor hormones in anesthetized and conscious rats
Authors: Leskinen H. , Ruskoaho H. , Huttunen P. , Leppaluoto J. , Vuolteenaho O.
Published: December 2017

We examined the effect of hemorrhage on plasma NH2-terminal pro-atrial natriuretic peptide (NT-pro-ANP) and atrial natriuretic peptide (ANP) in anesthetized and conscious rats. Blood (1.5 ml/time point) was withdrawn at 0, 10, 20, and 30 min. In anesthetized rats it caused decrease in mean arterial pressure and led to bradycardia in 2 min. Right atrial pressure decreased significantly after 12 min. However, plasma ANP did not change, and NT-pro-ANP actually increased from 481 +/- 55 to 609 +/- 73 pmol/l (P < 0.01) at 20 min and to 696 +/- 82 pmol/l (P < 0.01) at 30 min. Also plasma arginine-8-vasopressin (AVP) and epinephrine increased significantly at 30 min. No significant changes in plasma endothelin and norepinephrine were found. The increase in NT-pro-ANP after hemorrhage was not blocked by AVP V1-receptor, alpha- and beta-catecholaminergic receptor, or muscarinic-receptor antagonists. The plasma 125I-ANP disappearance curve was shifted to the right after hemorrhage in anesthetized rats, suggesting that the elimination of ANP was decreased. In conscious rats, heart rate and right atrial pressure did not change significantly after hemorrhage, and mean arterial pressure did not decrease until 22 min. NT-pro-ANP decreased from 1,467 +/- 146 to 1,072 +/- 130 pmol/l (P < 0.01) at 20 min and to 941 +/- 41 pmol/l (P < 0.01) at 30 min. Plasma ANP did not respond to hemorrhage in conscious rats. In conclusion, we found no change in plasma ANP during hemorrhage in either anesthetized or conscious rats, but we did find a significant increase in plasma NT-pro-ANP levels in anesthetized rats and a significant decrease in conscious rats. We suggest that this divergence may be due to different hemodynamic responses to hemorrhage.
Effect of chronic ANG I-converting enzyme inhibition on aging processes. III. Endothelial function of mesenteric arterial bed of rat
Authors: Atkinson J. , Tatchum-Talom R. , Corman B.
Published: December 2017

Age-related changes in endothelial (E) function were studied in mesenteric arterial bed (MAB) preparations removed from male, normotensive, WAG/Rij rats. At the age of 6 mo, one-half of the animals was assigned to chronic treatment with a hypotensive dose of an angiotensin I (ANG I)-converting enzyme inhibitor (ACEI; perindopril, 1 mg.kg-1.day-1 po). Animals were killed at 6, 12, 24, or 30 mo of age; the MAB was perfused in vitro, perfusion pressure (PP) being taken as an index of arteriolar tone. Disruption of E function produced a fall in baseline PP in all groups except 30-mo-old rats, suggesting that 1) baseline tone is maintained by the release of E vasoconstrictor factor(s) and 2) this mechanism is impaired in 30-mo-old rats. The muscarinic agonist, carbachol, antagonized vasoconstriction produced by norepinephrine (NE) in the presence of E. This mechanism was impaired in 30-mo-old rats. NE vasoconstriction increased following disruption of E, suggesting that NE release of endothelium-derived relaxing factor attenuates vasoconstriction. This mechanism was impaired in 30-mo-old rats. Chronic ACEI postponed the age-related decrease in E function, possibly due to a direct effect, or an indirect effect via the prolonged hypotensive action of such treatment.
Somnogenic effects of rabbit and recombinant human interferons in rabbits
Authors: Kimura M. , Majde J. A. , Toth L. A. , Opp M. R. , Krueger J. M.
Published: December 2017

Interferons (IFNs) are antiviral cytokines that possess several central nervous system activities. IFN therapy is associated with sleepiness, and the IFNs expressed during viral infection may be involved in the excess sleep associated with these infections. Most viruses stimulate the production of both IFN-alpha and IFN-beta. Although large doses of human IFN-alpha 2 are somnogenic in rabbits, the effects of species-specific IFNs on sleep in the rabbit have not been documented. We compared the somnogenic and antiviral effects of IFNs derived from rabbits to the effects of recombinant human (rh) IFN-alpha and IFN-beta. When injected intracerebroventricularly, rhIFN-alpha A/D, rabbit IFN-alpha/beta, and rabbit reference IFN induced non-rapid-eye-movement sleep and fever in a dose-dependent manner. However, the doses of rabbit IFNs required to induce sleep were much lower than those of human IFNs. Heat treatment of both rabbit IFNs and human IFNs greatly reduced their in vitro antiviral effects. The in vivo activities of rabbit IFNs and rhIFN-alpha A/D were significantly attenuated after heat treatment. However, rhIFN-beta retained its sleep-promoting action after heat treatment, suggesting that microbial contaminants were responsible for its somnogenic and pyrogenic activities. We conclude that IFN-alpha is somnogenic.
Soleus muscle contractile properties in hypertensive rats
Authors: Gray S. D. , Carlsen R. C. , Deng J.
Published: December 2017

Three types of hypertensive rats, and their normotensive controls, were assessed to determine the effects of high blood pressure on the contractile and fatigue properties of the soleus muscle. Spontaneously hypertensive rat (SHR) soleus developed less contractile force and fatigued more rapidly than normotensive Wistar-Kyoto (WKY) controls. In contrast, normotensive Wistar and Wistar-1 kidney/1 renal clip hypertensives were similar in their responses, and Dahl salt-sensitive hypertensives and Dahl salt-resistant controls also did not exhibit any significant differences in tension development or endurance. The results suggest that the decreased ability to develop force and maintain it during stimulation may not be directly related to the high blood pressure in SHR. It may instead be related to a gene defect that cosegregates with the loci responsible for the rise in blood pressure. The reduced endurance in SHR may be associated with an increased accumulation of K+ in the muscle during contraction, which decreases performance. It may also decrease the ability of the vessels to dilate during muscle contraction, preventing maintenance of an adequate blood supply.
Exercise-induced changes in blood composition of racing reindeer (Rangifer tarandus tarandus L.)
Authors: Poso A. R. , Nieminen M. , Sankari S. , Soveri T.
Published: December 2017

The responses to near-maximal exercise before and after the training and racing season were examined in reindeer. The reindeer were tested when pulling a driver at a speed of 11-12 m/s for 600 m. The lactate responses were higher before than after training. Similarly, the accumulation of uric acid, a breakdown product of ATP, became attenuated after training. The serum concentrations of nonesterified fatty acids decreased or did not change after exercise, although an increase in the glycerol concentration indicates activation of lipolysis. The concentration of alanine increased after both tests, and at rest the concentrations of several amino acids, e.g., glutamine, isoleucine, and tyrosine, were higher and the concentrations of serum protein and urea were lower during spring than at the beginning of the training period. It can be concluded that the carbohydrate metabolism of the reindeer responds to exercise and training similarly to that in other athletic species, but further studies are needed to explain the observed changes in lipid and protein metabolites.
Lack of increase in platelet Ca2+ and Na+ in deoxycorticosterone acetate-salt hypertensive rats
Authors: Ishida M. , Ishida T. , Matsuura H. , Ozono R. , Kajiyama G. , Oshima T.
Published: December 2017

We have previously characterized abnormal Ca2+ handling in platelets of spontaneously hypertensive rats (SHRs). In this study, we investigated whether cellular Ca2+ metabolism and/or Na+ concentration is altered in platelets of deoxycorticosterone acetate-salt hypertensive rats (DOCA rats). The resting cytosolic Ca2+ concentration ([Ca2+]i) in platelets was significantly lower in DOCA rats than controls (54.5 +/- 1.4 vs. 61.2 +/- 2.3 nmol/l). The amplitude of the [Ca2+]i transient induced by thrombin was significantly increased in the absence, but not the presence, of external Ca2+ in DOCA rats compared with control rats. The [Ca2+]i response to 5 mumol/l ionomycin in the Ca(2+)-free buffer was greater in DOCA rats than in controls (546 +/- 23 vs. 470 +/- 18 nmol/l), indicating larger intracellular Ca2+ stores. The rate of recovery of [Ca2+]i after the peak response to thrombin was decreased in DOCA rats (79% at 0.1 U/ml and 91% at 1.0 U/ml thrombin of control rats). Cytosolic Na+ concentration ([Na+]i) in platelets was similar in DOCA and control rats. Altered Ca2+ levels are not correlated with [Na+]i in this salt-sensitive hypertensive model. Therefore, an increased [Ca2+]i is not an obligatory phenomenon in hypertension.
Autonomic responses of the insular cortex in hypertensive and normotensive rats
Authors: Butcher K. S. , Cechetto D. F.
Published: December 2017

Lesion and focal cerebral ischemia of the insular cortex (IC) results in elevated renal sympathetic nerve activity (RSNA) and arterial pressure (AP) in the Wistar rat, while the opposite effect is observed in the spontaneously hypertensive rat (SHR). Acute changes in AP, heart rate (HR) and RSNA were measured in propofol-anesthetized and conscious SHR (n = 17) and Wistar rats (n = 17) during pressure injection of D,L-homocysteic acid (DLH; 100 mM) and lidocaine (LID; 20 mg/ml) into the IC. DLH injections (200 nl) into the IC of anesthetized Wistar rats resulted in a significant increase in MAP (mean change = +27 +/- 7 mmHg; P < 0.05) and a significant decrease in HR (-22 +/- 9 beats/min) and RSNA (-11 +/- 4 microV.s). Neither DLH nor LID injections into the IC of anesthetized SHR affected MAP or RNA. DLH and LID injections (500 nl) into the IC of conscious Wistar rats both resulted in a significant increase in MAP (+26 +/- 5 mmHg; 11 +/- 4 mmHg, respectively). Neither DLH nor LID injections had any cardiovascular effects in the conscious SHR. It therefore appears that the IC of conscious Wistar rats has a tonic inhibitory output, while neural excitation is capable of eliciting pressor responses. Conversely, the IC of SHR appears to exert no tonic influence on MAP.
Chronic endothelin-induced pressor and renal actions in conscious dogs do not require altered ANG II formation
Authors: Wilkins F. C. , Kassab S. , Kato T. , Mizelle H. L. , Opgenorth T. J. , Granger J. P.
Published: December 2017

Plasma endothelin levels are elevated approximately two- to threefold in a number of chronic pathophysiological conditions associated with hypertension. Results from recent studies indicate an important interaction between endothelin and the renin-angiotensin system (RAS). The role of the RAS in mediating the increases in arterial pressure produced by long-term pathophysiological elevations in circulating levels of endothelin is unknown. Therefore, the purpose of this study was to chronically increase circulating levels of endothelin within the pathophysiological range and determine the long-term cardiovascular and renal actions of endothelin in control dogs (n = 6) and in dogs pretreated with a converting-enzyme inhibitor (CEI) (n = 6) or CEI + angiotensin II (ANG II) replacement (n = 6). Infusion of endothelin-1 for 8 days at a rate of 2.5 ng.kg-1.min-1 increased plasma endothelin from 7.1 +/- 0.9 to 19.8 +/- 3.3 pg/ml. In control dogs, endothelin increased mean arterial pressure (MAP) by 19% (90 +/- 2 to 107 +/- 3 mmHg) while decreasing renal blood flow (RBF) by 30% and glomerular filtration rate (GFR) by 15-20%. Long-term elevation of circulating endothelin produced similar elevations in MAP in dogs pretreated with CEI (+16%) or CEI + ANG II (+17%). Similar decreases in RBF and GFR also occurred in response to endothelin in all three groups. These results indicate that although long-term increases in circulating endothelin within the pathophysiological range produce significant increases in arterial pressure, this effect does not appear to be mediated by the RAS.
Role of corticosterone in TNF and IL-6 production in isolated perfused rat liver
Authors: Liao J. , Keiser J. A. , Scales W. E. , Kunkel S. L. , Kluger M. J.
Published: December 2017

Using an isolated perfused rat liver (IPRL) preparation, we assessed whether corticosterone may contribute to the rise in tumor necrosis factor (TNF) and interleukin-6 (IL-6) in rats after injection with lipopolysaccharide (LPS) or exposure to psychological stress. Intravenous infusion of LPS into the IPRL led to dose-dependent increases in TNF and IL-6 concentrations in the effluent. Anisomycin, a protein synthesis inhibitor, completely blocked the rise in TNF and IL-6 concentration in the IPRL effluent, supporting the hypothesis that the synthesis (or release) of these cytokines was dependent on protein synthesis. Intravenous infusion of corticosterone at nonstressed (35 ng/ml) and stressed levels (350 ng/ml) increased TNF and/or IL-6 release. However, when LPS was combined with corticosterone, the lower dose of corticosterone facilitated the release of cytokines, whereas the higher dose of corticosterone suppressed the release of cytokines. We then showed that isolated Kupffer cells were capable of significant TNF and IL-6 production and that corticosterone decreased LPS-induced cytokine production in these cells. Our data support the hypothesis that the liver is an important source of circulating cytokines in response to LPS. In addition, although in vitro data generally support the hypothesis that corticosterone suppresses the production of cytokines, our in situ data support the hypothesis that physiological levels of corticosterone cause an increase in TNF and IL-6.
Metabolic, hormonal, and hemodynamic changes induced by metabotropic excitatory amino acid agonist (1S,3R)-ACPD
Authors: Lang C. H. , Ajmal M.
Published: December 2017

The purpose of the present study was to determine whether central administration of (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD), a selective metabotropic glutamate receptor agonist, would stimulate glucose metabolism, activate the hypothalamic-pituitary-adrenal axis, or influence pancreatic endocrine secretion. Intracerebroventricular injection of ACPD increased arterial glucose levels by 60% within 15 min, which were sustained throughout the 3-h experimental protocol. This hyperglycemia resulted from an early increase in hepatic glucose production (HGP, 88%) that exceeded the increase in glucose uptake by peripheral tissues (66%). Stimulation of glucose metabolism was associated with transient elevations in plasma insulin (145%) and glucagon (3-fold) levels and more sustained elevations in corticosterone (141%), epinephrine (3- to 5-fold), and norepinephrine (32-110%). Intravenous infusion of alpha- and beta-adrenergic antagonists prevented the ACPD-induced increase in glucose metabolism. Arterial blood pressure, cardiac index, and total peripheral resistance were not altered after ACPD. Overall, the changes in regional blood flow were unremarkable, although ACPD did increase blood flow to the liver (2-fold) and heart (48%) and decrease flow to the stomach (33%). These results indicate that central administration of ACPD 1) enhances HGP, which is primarily mediated by adrenergic stimulation; 2) increases glucose uptake by peripheral tissues, which appears to be mediated by both hyperinsulinemia and hyperglycemia; 3) stimulates pancreatic and adrenal hormone secretion independent of adrenergic activation; and 4) produces minimal changes in regional blood flow that cannot explain the glucose metabolic response produced by ACPD.(ABSTRACT TRUNCATED AT 250 WORDS)
Alterations in the insulin-like growth factor system in trauma patients
Authors: Wojnar M. M. , Fan J. , Frost R. A. , Gelato M. C. , Lang C. H.
Published: December 2017

The aim of the present study was to elucidate changes in the growth hormone (GH)-insulin-like growth factor (IGF) axis in trauma patients throughout their stay in the surgical intensive care unit (SICU). The first venous blood sample was obtained within 24 h after admission to the SICU and before the start of nutritional support; the last sample was obtained within 24 h of each patient's discharge from the SICU. All patients were receiving nutritional support at this later time. Control subjects were healthy volunteers, matched for age and sex and fasted approximately 18 h before blood sampling. GH in trauma patients was increased 25-fold on the first day and was still elevated > or = 5-fold on the last day. Trauma decreased circulating levels of both IGF-I (50-60%) and IGF-II (33-45%) throughout the duration of the patients' stay in the SICU. A sustained reduction in plasma IGF-binding protein (BP)-3 (55-75%) was observed in trauma patients throughout the protocol. In contrast, IGFBP-1 levels increased more than threefold during this same period. Furthermore, IGFBP-1 in these patients had undergone posttranslational modification and existed primarily in a highly phosphorylated form. Blood, collected from a cohort (n = 3) of these patients within 24 h of their discharge from the hospital, indicated that IGF-I and IGF-II were still reduced (30%) and that the decrease in IGFBP-3 and the elevation in IGFBP-1 were still evident at this time.(ABSTRACT TRUNCATED AT 250 WORDS)
Nitric oxide contributes to functional hyperemia in cerebellar cortex
Authors: Iadecola C. , Li J. , Ebner T. J. , Xu X.
Published: December 2017

We used the parallel fibers (PF) system of the cerebellar cortex as a model to investigate the role of nitric oxide (NO) in the increases in blood flow elicited by neural activation. Rats were anesthetized with halothane and ventilated. The vermis was exposed, and the site was superfused with Ringer (37 degrees C; pH 7.3-7.4). PF were stimulated electrically (100 muA; 30 Hz), and the associated changes in cerebellar cortex blood flow (BFcrb) were monitored by laser-Doppler flowmetry. The field potentials evoked by PF stimulation were recorded using microelectrodes. During Ringer superfusion (n = 7), PF stimulation increased BFcrb (+ 52 +/- 4%). Topical application of the NO synthase (NOS) inhibitor N omega-nitro-L-arginine (L-NNA; 0.1-1 mM) attenuated the increases in BFcrb dose dependently and by 50 +/- 4% at 1 mM (n = 9; P < 0.001; analysis of variance and Tukey's test). L-NNA (1 mM) inhibited NOS catalytic activity, assessed ex vivo using the citrulline assay, by 95 +/- 9% (P < 0.001). L-NNA did not influence the field potentials evoked by PF stimulation. D-NNA (1 mM; n = 6), the inactive stereoisomer of nitroarginine, did not attenuate the BFcrb response (P > 0.05). Methylene blue (1 mM; n = 7) reduced the response by 41 +/- 9% (P < 0.01) without affecting NOS catalytic activity (P < 0.05). The increases in BFcrb were not affected by lesioning the NOS-containing nerve fibers innervating cerebral vessels, indicating that these nerves are not the source of NO. Thus the increases in BFcrb elicited by activation of PF are, in part, mediated by NO produced in the molecular layer during neural activity. The results indicated that NO participates in the coupling of function activity to blood flow and support the hypothesis that NO is one of the mediators responsible for functional hyperemia in the central nervous system.
Low-frequency subthreshold sympathetic stimulation augments maximal reflex parasympathetic salivary secretion in cats
Authors: Izumi H. , Karita K.
Published: December 2017

Electrical stimulation of the peripheral cut end of the cervical sympathetic trunk for 3 min at frequencies < 1 Hz with pulses of 2-ms duration at supramaximal intensities did not elicit any salivary secretion, but an increase of stimulus frequency over the range 2-10 Hz produced progressively greater salivary secretion, the maximum volume of salivary secretion being evoked at 10 Hz. Frequency-dependent augmentation of parasympathetic reflex submandibular salivary secretion occurred when the lingual nerve was stimulated during repetitive sympathetic stimulation (at frequencies of 0.1-2 Hz) in our sympathectomized cats. The augmentation was found to be linearly related to sympathetic stimulus frequency (regression line calculated by method of least squares; r = 0.939, P < 0.01). This augmentation was abolished by prior treatment with the beta-adrenoceptor blocking drug propranolol (1 mg/kg, P < 0.01 vs. before propranolol) but not by the alpha-adrenoceptor blocking agent phentolamine (1 mg/kg), indicating that the augmented response was mediated via an activation of beta-adrenoceptors. The reduction of the augmentation caused by propranolol had diminished 1 h after its administration, showing that the effect was reversible.
Poly I:C-induced fever elevates threshold for shivering but reduces thermosensitivity in rabbits
Authors: Toien O. , Mercer J. B.
Published: December 2017

Shivering threshold and thermosensitivity were determined in six conscious rabbits at ambient temperature (Ta) 20 and 10 degrees C before and at six different times after saline injection (0.15 ml iv) and polyriboinosinic-polyribocytidylic acid (poly I:C)-induced fever (5 micrograms/kg iv). Thermosensitivity was calculated by regression of metabolic heat production (M) and hypothalamic temperature (Thypo) during short periods (5-10 min) of square-wave cooling. Heat was extracted with a chronically implanted intravascular heat exchanger. Shivering threshold was calculated as the Thypo at which the thermosensitivity line crossed resting M as measured in afebrile animals at Ta 20 degrees C. There were negligible changes in shivering threshold and thermosensitivity in saline-injected rabbits. In the febrile animals, shivering threshold generally followed the shape of the biphasic fever response. At Ta 20 degrees C, shivering threshold was higher than regulated Thypo during the initial rising phase of fever and was lower during recovery. At Ta 10 degrees C the shivering thresholds were always higher than regulated Thypo except during recovery. Thermosensitivity was reduced by 30-41% during fever.
Role of ventrolateral medulla in reflex cardiovascular responses to activation of skin and muscle nerves
Authors: Ruggeri P. , Ermirio R. , Molinari C. , Calaresu F. R.
Published: December 2017

Central neuronal circuits mediating reflex cardiovascular responses to skin and muscle nerve stimulation were studied in rats under urethan anesthesia. Responses of right rostral ventrolateral medulla (RVLM) and caudal ventrolateral medulla (CVLM) cardiovascular neurons to stimulation of contralateral skin and muscle afferent fibers were investigated. Stimulation of the tibial (muscle) nerve excited 19 (86%) of 22 CVLM neurons and inhibited 18 (82%) of 22 RVLM neurons. Stimulation of the sural (skin) nerve excited 20 (91%) of the 22 RVLM neurons but did not affect the firing rate of any of the 22 CVLM neurons. Electrolytic lesions of the CVLM abolished the depressor responses induced by stimulation of the tibial nerve without affecting the pressor response caused by sural nerve stimulation. Similarly, reversible blockade of the CVLM by microinjection of gamma-amino-butyric acid or CoCl2 abolished the depressor response to stimulation of the tibial nerve without affecting the pressor response induced by sural nerve stimulation. These results suggest that vasodepressor responses to muscle nerve activation are mediated by a neuronal inhibitory pathway to the RVLM relayed through the CVLM.
Effects of hypoxia and hypercapnia on whole body release and clearance of choline
Authors: Jenden D. J. , Scremin O. U.
Published: December 2017

We have recently demonstrated an increase in arterial blood choline (Ch) concentration in normocapnic hypoxia and apnea. This could be due to enhanced release of free Ch from tissues, to decreased Ch clearance, or both. The present investigations was undertaken to determine the individual contributions of these processes to the whole body balance of Ch, using an intravenous infusion of tracer quantities of [2H4]Ch to assess the bidirectional flux between the central pool and peripheral pools. Rats were subjected to normocapnic hypoxia or hypercapnia; release and clearance of Ch were calculated using a simple model. Hypoxia caused an increase in Ch production and a decrease in Ch clearance. At severe levels of hypoxia, Ch clearance was essentially zero. Hypoxia was attended by progressive acidosis that was related to the magnitude of the hypoxic challenge. To determine the possible effects of acidosis per se on the variables measured, respiratory acidosis with normoxia was provoked by controlled administration of CO2. Under these conditions, parallel decreases in Ch production and Ch clearance were observed.
Behavior of sheep drinking ethanol solution
Authors: Blair-West J. R. , Deam D. R. , Denton D. A. , Tarjan E. , Weisinger R. S.
Published: December 2017

Sheep that were habituated to drinking 10% (vol/vol) ethanol solution instead of water were subjected to proven thirst stimuli to study the effect of chronic ethanol intake on brain mechanisms subserving thirst. Sheep that had not previously drunk 10% ethanol were also tested. All sheep were trained to press a pedal that delivered 50 ml/press of fluid (either 10% ethanol or water) into a drinking cup. In some experiments, fluids were presented in bins. All animals had access to only one fluid at a time. Five ethanol-drinking sheep appeared healthy and maintained body weight over 18 mo. They always preferred water to 10% ethanol. The intracerebroventricular (icv) infusion of angiotensin II (ANG II) at 3.8 micrograms/h for 2 h increased ethanol intake from 15 +/- 10 to 200 +/- 55 ml in the 1st h, but 2,850 +/- 320 ml of water was drunk in the 2nd h. The icv infusion of 500 mM NaCl had a similar effect. After fluid deprivation for 22 or 46 h, ethanol intake in 1 h of access was only 280 +/- 40 and 400 +/- 90 ml, respectively, and 24-h intake was not increased. Water-drinking sheep drank 1,300 +/- 195 ml of water in 1 h after 22-h water deprivation, and 24-h intake was 1.5 times normal. The icv infusion of ANG II in these sheep increased water intake in 1 h from 10 +/- 10 to 1,630 +/- 250 ml and intake of 10% ethanol to only 310 +/- 60 ml. In conclusion, sheep accept 10% ethanol as a substitute for water for daily drinking.(ABSTRACT TRUNCATED AT 250 WORDS)
Serotonin enhances gastric acid response to TRH analogue in dorsal vagal complex through 5-HT2 receptors in rats
Authors: Yoneda M. , Tache Y.
Published: December 2017

The effect of serotonin (5-HT) and thyrotropin-releasing hormone (TRH) analogue, p-Glu-His-[3,3'-dimethyl]-Pro-NH2 (RX-77368), injected into the dorsal vagal complex (DVC) on gastric acid secretion was assessed in urethan-anesthetized rats with gastric cannula. 5-HT (0.1, 0.2, 1, or 10 nmol into the DVC) enhanced the acid response to RX-77368 (25 pmol, DVC) by 54, 100, 147, and 144%, respectively, whereas 5-HT given alone had no effect. The 5-HT2 receptor agonists (1 nmol, DVC), ( +/- )-1-(4-iodo-2,5-dimethoxyphenyl)-2-aminopropane hydrochloride, 1-(alpha, alpha, alpha-trifluoro-m-tolyl)-piperazine hydrochloride, and alpha-methyl-5-HT increased the gastric acid response to coinjection of RX-77368 (25 pmol) by 153, 108, and 96%, respectively, whereas 8-hydroxy-2-(di-n-propylamino)tetralin (5-HT1A), 7-trifluoromethyl-4(4-methyl-1-piperazinyl)- pyrrolo[1,2-a]quinoxaline (5-HT1A/1B), and 3-(2-aminoethyl)-2-methyl-1-H-indol-5-ol hydrochloride hydrate (2-methyl-5-HT3) did not. The 5-HT2 receptor antagonist, 3-[2-(4-fluorobenzoyl)-1-piperdinyl]ethyl]-2,4(1H,3H)-quinazoli nedone tartrate (ketanserin; 20 nmol), injected intracisternally abolished the potentiating action of 5-HT injected into the DVC with RX-77368, whereas the 5-HT antagonists 8-[4-(4-fluorophenyl)-4-oxobutyl]-1-phenyl-1,3,8-triazaspiro[4,5]- decan-4-one (spiperone; 5-HT2/1A) and 1,2,3,9-tetrahydro-9-methyl-3-[(2-methyl-1H-imidazol-1- yl)methyl]-4H-carbazol-4-one hydrochloride dihydrate (ondansetron; 5-HT3) did not. Ketanserin (1 nmol/site bilaterally into the DVC) decreased the acid response to kainic acid injected into the raphe pallidus by 62%. These data suggest that 5-HT acting at 5-HT2 receptors in the DVC potentiates the gastric acid response to exogenous and endogenous TRH.
Effects of duodenal and distal ileal infusions of glucose and oleic acid on meal patterns in rats
Authors: Woltman T. , Reidelberger R.
Published: December 2017

The mechanisms mediating the anorexic effects of nutrients in the proximal and distal small intestine are not clearly understood. We determined the dose-dependent effects of duodenal and distal ileal infusions of glucose and oleic acid on meal patterns in ad libitum feeding rats. Rats with cannulas in both the duodenum and ileum received a 2-h infusion of glucose (0, 800, 1,600, 3,200, 6,400, or 12,800 mumol/h) or oleic acid (0, 48, 240, 640, or 1,280 mumol/h) into the duodenum or ileum at the start of the dark period, and meal patterns were monitored for 4 h. Cumulative food intake was inhibited dose dependently by ileal as well as duodenal infusion of both glucose and oleic acid. Ileal glucose was more inhibitory than duodenal glucose, whereas duodenal oleic acid was more inhibitory than ileal oleic acid. Duodenal glucose and oleic acid inhibited feeding by decreasing meal frequency; ileal oleic acid decreased only meal size, whereas ileal glucose reduced both meal size and frequency. We interpret these results to suggest that ileal oleic acid and glucose suppress feeding by different mechanisms and that these mechanisms differ from those mediating the anorexic responses to oleic acid and glucose in the duodenum.
Effect of local warming on hand and finger artery blood velocities
Authors: Bergersen T. K. , Eriksen M. , Walloe L.
Published: December 2017

The effect of local heating on blood velocities in arteries supplying the skin of hand and fingers was studied in subjects kept in their thermoneutral zone. The temperature of one hand was steadily raised from 35 to 43 degrees C in 15 min, whereas the control hand was kept in the air or immersed in a water bath at 35 degrees C. Simultaneous blood velocity recordings from the two hands were made continuously using ultrasound Doppler. In the heated hand, a general rise in blood velocity level was seen. However, the spontaneous fluctuations in blood velocity assumed to be caused by synchronous vasomotor activity of the arteriovenous anastomoses (AVAs) remained unchanged and closely correlated with those in the control hand throughout the experiment. Thus the central nervous control of AVA vasomotion seems to be unaffected by local heating. The elevation of blood velocity in the heated hand is probably due to dilatation of other parts of the vascular bed, e.g., ordinary arterioles in the skin. Earlier investigators, using venous occlusion plethysmography, have reported vasoconstriction in the locally heated human finger. No sign of such heat-induced vasoconstriction was found in this study.
Fundus striati vasopressin receptors in blood pressure control
Authors: Kremarik P. , Freund-Mercier M. J. , Pittman Q. J.
Published: December 2017

Vasopressin (VP), given intracerebrally to rats, can induce antipyresis, motor disturbances, and increases in arterial blood pressure. The possibility that the VP-binding sites in the fundus striati (FStr) could participate in these effects was investigated. After a bilateral injection of 100 pmol of VP into the FStr, the fever induced by an injection of the lipopolysaccharide of Escherichia coli (50 micrograms/kg ip) was not affected. Bilateral injections of 100 pmol of VP did not induce motor disturbances or alterations in body temperature after either of two successive injections. In contrast, bilateral injections of VP into urethan-anesthetized rats induced dose-dependent increases in arterial pressure without affecting heart rate. This increase was blocked by a V1 antagonist; oxytocin and a V2 agonist were ineffective. In keeping with this preliminary pharmacological analysis, radio-ligand-binding studies of the FStr revealed binding sites in the FStr exhibiting a binding profile typical of the V1 subtype. This study suggests that the V1 receptors in the FStr could participate in the central regulation of the blood pressure.
Na-D-glucose cotransport in renal brush-border membrane vesicles of an early teleost (Oncorhynchus mykiss)
Authors: Freire C. A. , Kinne-Saffran E. , Beyenbach K. W. , Kinne R. K.
Published: December 2017

Brush-border membrane vesicles (BBMV) enriched with alkaline phosphatase (8.1-fold) and gamma-glutamyl transpeptidase (11.5-fold) were prepared from the rainbow trout kidney. D-[3H]glucose uptake was stimulated by inward Na gradients but not by K, choline, Li, N-methyl-D-glucamine, or mannitol gradients. Na-dependent glucose uptake displayed overshoot in voltage-polarized vesicles (VPV; negative inside) but not in short-circuited vesicles (SCV). Recognition of carbons 2 and 3 of the glucopyranose ring was essential for glucose uptake. Phlorizin inhibited Na-dependent D-glucose uptake with an inhibition constant of 11.4 microM. The Michaelis-Menten constant of glucose was 0.58 mM in VPV and increased to 1.49 mM in SCV, whereas that for sodium was 193 mM in VPV and similar in SCV. Maximum velocity of Na was reduced in SCV. The Hill coefficient was 1 for both Na and glucose in VPV and SCV. Our studies indicate a single Na-D-glucose cotransporter that transports Na and glucose with a 1:1 stoichiometry and voltage-dependent kinetics. The transporter shares functional properties with both mammalian transporters SGLT1 and SGLT2.
Lesion of central nucleus of amygdala promotes fat gain without preventing effect of exercise on energy balance
Authors: Bovetto S. , Richard D.
Published: December 2017

Male Wistar rats with intact or lesioned central nucleus of amygdala (CeA) were kept at rest or subjected to a treadmill running program for 21 consecutive days. Food intake and body weight were monitored throughout the exercise training program. At the end of the program, rats were killed and their carcasses processed for analysis of the contents in energy, fat, and protein. Exercise and CeA lesions induced opposite effects on energy balance; exercise delayed gains in body energy and fat, whereas CeA lesions promoted them. Total energy intake was lower in exercised rats than in sedentary ones over the 12 and 24 h that followed exercise. Food intake was higher in lesioned rats than in intact animals over the second half of the 12-h period that followed exercise. There was no interaction effect of exercise and CeA lesions on energy balance and intake and on body composition. Plasma levels of adrenocorticotropin hormone and corticosterone were higher in exercised rats than in sedentary ones, but there was no difference between lesioned and intact rats. This study, as well as confirming the effect of exercise on energy balance, indicates that CeA lesions may promote energy deposition in rats. Above all the present results provide evidence that CeA does not represent a necessary neuroanatomic structure in the effect of exercise on energy balance.
Role of serotonergic neurons in the maintenance of the 10-Hz rhythm in sympathetic nerve discharge
Authors: Orer H. S. , Clement M. E. , Barman S. M. , Zhong S. , Gebber G. L. , McCall R. B.
Published: December 2017

We studied the effects of serotonin (5-HT)-receptor agonists and antagonists on the naturally occurring 10-Hz rhythm in sympathetic nerve discharge (SND) of urethan-anesthetized, baroreceptor-denervated cats. Intravenous doses of the 5-HT1A-receptor agonists 8-hydroxy-2(di-n-propylamino)-tetralin (8-OH-DPAT) and U-93385E, which inhibit the firing of serotonergic medullary raphe neurons, decreased the power in the 10-Hz band of SND without affecting the power at frequencies < or = 6 Hz. The inhibitory effects of 8-OH-DPAT and U-93385E were reversed by the 5-HT1A-receptor antagonists spiperone and WAY-100135. Microinjection of 8-OH-DPAT into medullary raphe nuclei also selectively eliminated the 10-Hz rhythm in SND. Intravenous administration of the 5-HT2-receptor antagonist methysergide blocked the 10-Hz rhythm in SND, whereas the 5-HT2-receptor agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane increased peak frequency and power in the 10-Hz band of SND. Microinjection of N-methyl-D-aspartic acid into the medullary raphe also enhanced the 10-Hz rhythm in SND. These data support the view that the naturally occurring discharges of serotonergic medullary raphe neurons preferentially enhance the 10-Hz rhythm in SND.
Involvement of type I corticosteroid receptor in the effects of ovariectomy on energy balance
Authors: Dagnault A. , Deshaies Y. , Richard D.
Published: December 2017

The effects of the glucocorticoid receptor antagonist, RU-38486 (RU-486), and the mineralocorticoid receptor (MR) antagonist, RU-28318, on energy balance were investigated in a 2 [surgery: ovariectomy (OVX) and sham operation] x 3 (corticosteroid antagonist: placebo, RU-28318, RU-486) experimental design. Rats were treated for 28 days. Food intake and body weight were monitored throughout the treatment period. At the end of the treatment, rats were killed and their carcasses were analyzed for energy and nitrogen contents. Energy content was determined by adiabatic bomb calorimetry, whereas nitrogen was determined in 250-to 300-mg samples of dehydrated carcasses, with the use of the Kjeldahl procedure. The energy as protein was subtracted from total carcass energy to determine energy as fat. The gains in energy, fat, and protein were calculated by subtracting the values obtained at the end of the treatment period from initial values estimated from the body weights measured at the beginning of the experiment. A significant interaction effect of surgery and corticosteroid antagonist was observed on body energy gain, energetic efficiency, and fat gain. Whereas body energy gain, energetic efficiency, and fat gain were larger in OVX rats than in sham-operated animals treated with either placebo or RU-486, they were comparable in OVX and sham-operated rats treated with RU-28318. Surgery, but not corticosteroid antagonist, had a significant effect on digestible energy intake, energy expenditure, and protein gain. All these variables were higher in OVX rats than in sham-operated animals. Surgery also affected corticosterone levels and adrenal weight. Both of these variables were lower in OVX rats than in sham-operated animals. By demonstrating the ability of RU-28318 to attenuate the effects of OVX on energy balance, the present study provides evidence that MR occupation by corticosteroids facilitates the OVX-induced changes in energy balance.
Opioid growth factor-dependent DNA synthesis in the neonatal rat aorta
Authors: Zagon I. S. , Wu Y. , McLaughlin P. J.
Published: December 2017

In addition to neuromodulation, endogenous opioids serve as growth factors in neural and nonneural cells. This study examined the hypothesis that opioids are inhibitory growth factors in vascular development. No circadian rhythm was detected for DNA synthesis in endothelial, smooth muscle, or fibroblast cells in the aorta of 1-day-old rats. Administration of naltrexone (NTX), a potent opioid antagonist, markedly increased the labeling indexes of all three cell types. [Met5]enkephalin, found to be the only opioid peptide to influence DNA synthesis and termed the opioid growth factor (OGF), depressed DNA synthesis in each cell type for 4-6 h in a dose-dependent and receptor-mediated manner. In aortas placed in tissue culture, DNA synthesis was significantly increased by incubation in NTX and decreased by incubation with OGF, Both OGF and its receptor, zeta (zeta), were associated with the cytoplasm of all three cell types in the neonatal aorta. These results indicate that an endogenous opioid peptide (i.e., OGF) and its receptor (i.e., zeta) reside in the developing vascular cells and govern DNA synthesis, with OGF acting directly as a tonic negative regulator of cell generation in the great vessels.
Access to rat kidney with minimal anesthesia and surgery: a new experimental model
Authors: Sadowski J. , Kompanowska-Jezierska E. , Walkowska A.
Published: December 2017

Chronic surgical explantation of the left rat kidney out of the abdominal cavity under the flank skin enabled easy access to the organ and ipsilateral urine collection under light chloralose anesthesia without virtually any surgical intervention. The glomerular filtration rate, urine flow and osmolality, sodium excretion, and medullary tissue hypertonicity were similar in the explanted and in the contralateral kidney, whereas p-aminohippurate clearance was 14% lower. The function of the explanted kidney was also compared with that of the kidney acutely exposed in rats under thiobutabarbital anesthesia and rendered euvolemic by isoncotic albumin infusion. Again, in both preparations renal function was comparable except that over time urine osmolality remained stable in the former and fell from 1,385 +/- 195 to 835 +/- 167 mosmol/kgH2O (P < 0.02) in the latter, indicating deterioration of urine concentration. Laser-Doppler probes could be easily applied in the explanted kidney to measure cortical and medullary blood flow. The new experimental model offers some advantages, both over studies using conscious rats and over experiments involving deep anesthesia and acute surgery.
Vasoactivity and immunoreactivity of fish tachykinins in the vascular system of the spiny dogfish
Authors: Kagstrom J. , Axelsson M. , Jensen J. , Farrell A. P. , Holmgren S.
Published: December 2017

Tachykinin control of gut blood flow (measured by pulsed Doppler technique), dorsal aortic pressure, and heart rate were studied in unrestrained spiny dogfish Squalus acanthias injected with the elasmobranch tachykinins scyliorhinin I and II (SCY I and SCY II), the trout tachykinins substance P (SP), and neurokinin A (NKA). Effects on somatic vasculature were measured by in vitro perfusion of the isolated tail. SCY I and trout SP produced hypotension due to a general vasodilation. This caused a transient increase in mesenteric blood flow and a prolonged increase in celiac blood flow. SCY II caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. Trout NKA evoked a short-lasting increase in celiac blood flow due to a decrease in vascular resistance, a late decrease in mesenteric flow due to vasoconstriction, and no effect on the somatic vasculature. None of the peptides affected heart rate. The study demonstrates a significant vasoactive function of fish tachykinins in the vascular system of an elasmobranch species and, in addition, the occurrence of tachykinin receptor subtypes. Immunohistochemistry revealed a NKA/SCY II-like peptide in nerve fibers innervating many vessels, including the celiac and the mesenteric arteries, the gastrointestinal canal, and the heart.
Membrane-metabolic coupling and ion homeostasis in anoxia-tolerant and anoxia-intolerant hepatocytes
Authors: Krumschnabel G. , Biasi C. , Schwarzbaum P. J. , Wieser W.
Published: December 2017

The relationship between membrane function and energy metabolism was studied in rainbow trout hepatocytes, an anoxia-intolerant cell system, and compared with the situation in hepatocytes from the goldfish, a typical anoxia-tolerant species. In trout hepatocytes, under normoxia and under chemical anoxia, inhibition of ATP consumption by the Na+ pump induced a decrease in ATP production of the same magnitude. In response to chemical anoxia, total ATP production was reduced to 15% and Na+ pump activity to 22% of the control rate under normoxia. Measurement of the cellular ATP content under these conditions revealed that, despite the reduction in Na+ pump activity, the cells became rapidly depleted of ATP, with the time course of this process resembling that observed in the anoxic rat hepatocyte. This is in contrast to the responses of goldfish hepatocytes, where, during chemical anoxia, 1) inhibition of the Na+ pump did not lead to a corresponding reduction in ATP production and 2) ATP levels, after a transient decrease, stabilized at a new steady state. To investigate the consequences of chemical anoxia on ion homeostasis, efflux and uptake rates of K+ were determined simultaneously. In the trout cells, chemical anoxia led to a decoupling of influx and efflux rates, the latter exceeding the former three- to eightfold. In contrast, goldfish hepatocytes were able to preserve ion homeostasis by a concerted decrease in Rb+ uptake and K+ efflux, so that the net flux of K+ was always close to zero. In neither species did chemical anoxia induce a change in pump density. Other potential control mechanisms are briefly discussed.
Histamine-sensitive intrinsic cardiac and intrathoracic extracardiac neurons influence cardiodynamics
Authors: Armour J. A.
Published: December 2017

Studies were performed to determine whether 1) histamine can modify the spontaneous activity of mammalian intrinsic cardiac neurons in situ, 2) histamine-sensitive neurons exist in intrathoracic intrinsic cardiac and extracardiac ganglia that are involved in cardiac regulation, and 3) histamine-sensitive intrathoracic cardiac neurons possess H1 or H2 receptors. histamine (10 microliters; 100 microM), when applied adjacent to spontaneously active canine right atrial neurons in situ, increased ongoing activity in some of them. Histamine, when administered into the local arterial blood supply of these neurons (0.1 ml; 100 microM) not only increased their activity but induced cardiac augmentation. Cardioaugmentor responses were also elicited when histamine (10 microliters or 0.1 ml; 100 microM) was administered into limited loci within stellate and middle cervical ganglia that were connected to the heart, but not in ganglia surgically disconnected the heart. Neuronal and cardiac responses no longer were elicited after local administration of the H1-selective receptor antagonist triprolidine. They were unaffected by local application of the H2-selective receptor antagonist cimetidine. No cardiac augmentation was elicited when histamine was applied to intrathoracic autonomic neurons following timolol (1 mg/kg i.v.) administration. These data indicate that 1) histaminergic neurons exist in intrinsic cardiac and intrathoracic extracardiac ganglia that are involved in cardiac regulation, 2) these neurons possess H1 receptors, and 3) histamine-sensitive intrathoracic neurons directly or indirectly activate cardiac adrenergic neurons, thereby inducing cardiac augmentation
Specificity of basolateral organic cation transport in snake renal proximal tubules
Authors: Kim Y. K. , Dantzler W. H.
Published: December 2017

We examined the specificity of basolateral organic cation transport in isolated snake (Thamnophis spp.) renal proximal tubules by determining the inhibitory effect of a series of n-tetraalkylammonium (n-TAA) compounds (n = 1-5) on the basolateral uptake of [3H]tetraethylammonium (TEA). The inhibitory potency increased with increasing alkyl chain length, with the apparent Michaelis constants for inhibition of TEA uptake ranging from 3.3 mM for tetramethylammonium (TMA) to 1.0 microM for tetrapentylammonium (TPeA). Thus the apparent affinity of the carrier for n-TAA compounds increases with their increasing hydrophobicity. Because previous data suggested that TEA transport across the basolateral membrane may be asymmetrical and that the exit step may be regulated differently from the entry step, we examined the kinetics of [3H]TEA efflux across the basolateral membrane, Efflux, like entry, occurred by a saturable process that could be described adequately by Michaelis-Menten kinetics. However, the concentration of TEA at one-half Jmax (Kt) for efflux (approximately 110 microM) was about six times the Kt for uptake (approximately 18 muM), indicating that the affinity of the carrier for TEA is greater in the uptake direction than in the efflux direction or that there are separate carriers with different affinities for uptake and efflux. In either case, this difference would favor movement of TEA taken up at the basolateral side across the cells and into the lumen over movement back into the peritubular fluid.