bluuebunny/crossref_metadata_2025 huggingface dataset:
Does the ovine placenta secrete ACTH under normoxic or hypoxic conditions?
Authors: Keller-Wood M. , Wood C. E.
Published: December 2017

In the sheep, maternal plasma cortisol is increased in late pregnancy, and fetal plasma cortisol and adrenocorticotropic hormone (ACTH) rise precipitously in late gestation. In many species, the placenta contains ACTH. These experiments were designed to test whether the ovine placenta contains ACTH and whether there is net secretion of ACTH by the uteroplacental unit into either the maternal or fetal circulation. Pregnant ewes and their fetuses were prepared with maternal and fetal arterial and uterine and umbilical venous catheters. Arterial and venous samples were taken from both sides of the placenta before and during hypoxia induced by the ewe breathing 9-11% O2, and arteriovenous (a-v) differences in ACTH, PO2, PCO2, and progesterone were analyzed. A positive a-v difference in PO2 (48.2 +/- 3.4 mmHg) and negative a-v differences in PCO2 and progesterone (-3.5 +/- 0.7 mmHg and -25 +/- 5 ng/ml, respectively) were found across the placenta in the ewe, and a positive a-v difference in PCO2 (4.8 +/- 0.9 mmHg) and negative a-v differences in PO2 and progesterone (-8.1 +/- 1.5 mmHg and -13 +/- 3 ng/ml, respectively) were found across the placenta in the fetus, indicating that the umbilical and uterine venous catheters were properly placed. Hypoxia decreased fetal and maternal arterial PO2 from 22.8 +/- 1.3 to 13.8 +/- 0.7 and from 98.8 +/- 3.3 to 37.0 +/- 2.6 mmHg, respectively, and increased fetal and maternal arterial ACTH immunoreactivity from 95 +/- 60 to 2,676 +/- 795 and from 149 +/- 21 to 275 +/- 88 pg/ml, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Organum cavum pre-lamina terminalis, an undescribed brain organ in rats: morphology and physiology
Authors: Nicolaidis S. , el Ghissassi M.
Published: December 2017

Morphological as well as physiological findings reported here point to the existence of a previously undescribed brain organ we refer to as the organum cavum pre-lamina terminalis (OCPLT). The organ is a hollow, sagittal, forebrain structure consisting of a vertical interhemispheric horn that overlies the anterior aspect of the lamina terminalis and a horizontal horn that lies in the septum below the corpus callosum. This horizontal horn was previously referred to as the cavum septi pellucidi, a vestigial anatomic curiosity. The narrow cavities of the horizontal and vertical horns join under the genu of the corpus callosum and communicate freely. The two horns do not communicate with the cerebral ventricular system or the subarachnoid spaces. Microinjections of greater than or equal to 0.2 ng angiotensin II into all regions of the cavity resulted in significant drinking, whereas injections into areas surrounding the cavities were ineffective. These data show that the organ is a discrete brain entity and displays high sensitivity to angiotensin II. These findings suggest that the OCPLT is another brain organ with significant effects on fluid and electrolyte homeostasis and perhaps other brain functions.
Salt appetite in rat pups: ontogeny of angiotensin II-aldosterone synergy
Authors: Thompson C. I. , Epstein A. N.
Published: December 2017

Preweanling rats were tested to determine whether angiotensin II (ANG II) and aldosterone (Aldo) act synergistically to enhance salt appetite at 12 and 17 days. Twelve-day-old pups received one of four hormone treatments in four doses: 1) ANG II only [1, 2, 10, or 100 ng pulse intracerebroventricular (icv)], 2) Aldo only (1, 2, 10, or 40 micrograms/day sc), 3) Aldo + ANG II (four individual doses combined), or 4) vehicle. Seventeen-day-old rats received the same treatments in two doses (2 or 100 ng ANG II; 2 or 40 micrograms Aldo). Pups were presatiated with milk through anterior oral catheters and then given either 4% NaCl or water for 30 min. Intake was assessed by body weight change. At both ages, ANG II enhanced salt (and water) intake, and Aldo enhanced salt (but not water) intake. Minimum effective doses were comparable to those reported for adults. ANG II-Aldo synergy was absent at 12 days and present at 17 days, when salt intake was 590% greater than the summed intakes evoked by ANG II and Aldo alone. The neural mechanisms for ANG II-Aldo synergy thus mature later than those mediating the hormone's individual actions in arousing salt appetite.
Receptor subtypes for natriuretic peptides in the brains of hypertensive rats
Authors: Brown J. , Czarnecki A.
Published: December 2017

Receptor subtypes for alpha-atrial natriuretic peptide (alpha-ANP) were characterized in brains of 12-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) by in vitro autoradiography, using des[Gln18, Ser19,Gly20,Leu21,Gly22]ANP-(4-23) (C-ANP) and ANP-(5-25) as subtype-selective ligands. 125I-labeled alpha-ANP (200 pM) bound reversibly to arachnoid mater (AM), choroid plexus (ChP), subfornical organ (SFO), median preoptic nucleus, and supraoptic nucleus. Apparent Kd values for alpha-ANP in AM, ChP, and SFO were 1-6 nM and they were lowest in SHR. Maximal binding capacities for alpha-ANP on ChP and SFO were also significantly lower in SHR, and 10 microM C-ANP or 10 microM ANP-(5-25) inhibited most radioligand binding on AM of WKY and SHR. C-ANP significantly inhibited no other alpha-125I-ANP binding. ANP-(5-25) was a relatively weak inhibitor of alpha-125I-ANP binding to ChP and SFO in WKY but it was powerful in SHR. The results suggest that AM expresses clearance receptor for alpha-ANP in WKY and SHR. Other structures do not express this receptor significantly but express two other receptors for alpha-ANP, one mainly in WKY and one mainly in SHR.
Interleukin 1-receptor antagonist blocks interleukin 1-induced sleep and fever
Authors: Opp M. R. , Krueger J. M.
Published: December 2017

The recent purification and characterization of an interleukin 1-receptor antagonist (IL-1ra) has provided an additional means of elucidating the mechanisms involved in the responses initiated by IL-1. Central administration of IL-1 to rabbits results in a characteristic febrile response and in increased non-rapid-eye-movement sleep (NREMS). In this study, rabbits received various doses of IL-1ra (10-1,000 micrograms) or pyrogen-free saline intracerebroventricularly, and sleep-wake activity and brain temperature (Tbr) were determined for the next 24 h. All doses of IL-1ra tested tended to reduce NREMS in the first postinjection hour with little effect on Tbr. When rabbits were pretreated with 100 micrograms IL-1ra and then injected with 10 ng IL-1, the characteristic IL-1-induced febrile and NREMS-promoting effects were completely blocked.
Morphine-induced activation of fetal EEG is mediated via central muscarinic pathways
Authors: Szeto H. H.
Published: December 2017

The effect of morphine on fetal electroencephalogram (EEG) was investigated using power spectral analysis. Morphine (0.15-5.0 mg/h) administered directly to the fetal lamb altered fetal EEG in three ways. First, morphine altered the relative incidence of the three preponderant EEG states [high-voltage slow activity (HVSA), transitional, and low-voltage fast activity (LVFA)]. Morphine resulted in a dose-dependent reduction in HVSA, with a reciprocal increase in transitional state at the lower doses and an increase in LVFA at higher doses. Second, morphine resulted in a more fragmented and unstable EEG pattern, with a significant increase in the number of state-to-state transitions. Third, there was a significant increase in the 90% spectral edge frequency as well as relative power distribution in the theta band. Taken together, these data suggest that morphine results in activation of the fetal EEG. This effect was completely abolished by concurrent intracerebroventricular administration of either methyl naloxone or methyl atropine, indicating that it is mediated by specific opioid receptors in the central nervous system and involves activation of central muscarinic pathways.
Distribution of dietary limiting amino acid injected into the prepyriform cortex
Authors: Beverly J. L. , Hrupka B. J. , Gietzen D. W. , Rogers Q. R.
Published: December 2017

Diffusion or metabolism of the dietary limiting amino acid (DLAA) in the prepyriform cortex (PPC) may account for the time lag between injection of the DLAA into the PPC and the increase in intake of an amino acid-imbalanced diet. Results from the injection of [3H]Leu +/- [14C]Thr (DLAA) into the PPC indicated rapid (less than 15 min) and limited diffusion (85-90% of recovered label was less than or equal to 1 mm from the injection site). 3H and 14C decreased in the trichloroacetic acid (TCA)-soluble fraction and increased in the TCA-insoluble fraction during the first 1.5 h and remained constant in the TCA-insoluble fraction 1.5-6 h after injection. An increase (approximately 50%) in 3H in the TCA-insoluble fraction was found less than or equal to 30 min after injection of the DLAA. There was no affect of the DLAA on 3H in the TCA-soluble fraction. These results indicated that a change in metabolism within the PPC may be responsible for the delay in onset of the feeding response after injection of the DLAA into the PPC.
Enhanced vagal baroreflex response during 24 h after acute exercise
Authors: Convertino V. A. , Adams W. C.
Published: December 2017

We evaluated carotid-cardiac baroreflex responses in eight normotensive men (25-41 yr) on two different test days, each separated by at least 1 wk. On one day, baroreflex response was tested before and at 3, 6, 12, 18, and 24 h after graded supine cycle exercise to volitional exhaustion. On another day, this 24-h protocol was repeated with no exercise (control). Beat-to-beat R-R intervals were measured during external application of graded pressures to the carotid sinuses from 40 to -65 mmHg; changes of R-R intervals were plotted against carotid pressure (systolic pressure minus neck chamber pressure). The maximum slope of the response relationship increased (P less than 0.05) from preexercise to 12 h (3.7 +/- 0.4 to 7.1 +/- 0.7 ms/mmHg) and remained significantly elevated through 24 h. The range of the R-R response was also increased from 217 +/- 24 to 274 +/- 32 ms (P less than 0.05). No significant differences were observed during the control 24-h period. An acute bout of graded exercise designed to elicit exhaustion increases the sensitivity and range of the carotid-cardiac baroreflex response for 24 h and enhances its capacity to buffer against hypotension by increasing heart rate. These results may represent an underlying mechanism that contributes to blood pressure stability after intense exercise.
Impairment of carotid-cardiac vagal baroreflex in wheelchair-dependent quadriplegics
Authors: Convertino V. A. , Adams W. C. , Shea J. D. , Thompson C. A. , Hoffler G. W.
Published: December 2017

The incidence of orthostatic hypotension can increase after prolonged exposure to chair rest and bedrest and is associated with post-bed rest impairment of the carotid-cardiac baroreflex response. We therefore hypothesized that the hypotension observed in humans confined to wheelchairs may be manifested by a reduced baroreflex sensitivity. We compared baroreflex responses of 16 wheelchair-dependent (WCD) quadriplegics with those of 15 able-bodied subjects (ABS) matched for age, height, and weight. Beat-to-beat R-R intervals were measured during application of graded pressures from 40 to -65 mmHg using a neck chamber for noninvasive stimulation of the carotid baroreceptors. Changes of R-R intervals were plotted against carotid distending pressures. The maximum slope of the stimulus-response relationship was greater (P less than 0.0001) in ABS (6.1 +/- 0.6 ms/mmHg) than in WCD (2.6 +/- 0.4 ms/mmHg). The range of the R-R interval response, i.e., the capacity to buffer blood pressure changes, was only 138 +/- 19 ms in WCD compared with 253 +/- 19 ms in ABS (P less than 0.001). Mean sitting systolic-to-diastolic blood pressures in WCD (92/60 mmHg) were less (P less than 0.0001) than in ABS (120/77 mmHg), although there were no significant differences between groups in supine resting blood pressures. Chronic loss of stimulation to carotid baroreceptors by routine standing posture is associated with attenuated sensitivity and reduced buffer capacity of the arterial baroreflex and hypotension during sitting in WCD patients.
Role of ventrolateral medulla in sympatholytic effect of 8-OHDPAT in rats
Authors: Nosjean A. , Guyenet P. G.
Published: December 2017

In halothane-anesthetized, paralyzed, and artificially ventilated rats, the putative 5-hydroxytryptamine1A receptor agonist 8-OHDPAT (13.1 micrograms/kg iv) produced hypotension (-14.6 +/- 1.3 mmHg, n = 35), reduced lumbar sympathetic nerve discharge (SND, -17.8%, n = 35), and slowed the discharge rate of sympathoexcitatory neurons recorded in the rostroventrolateral medulla (RVLM, -17.6%, n = 20). The gain of the baroreflex was unaffected by the drug, but SND and RVLM unit discharges were silenced at significantly reduced levels of mean arterial pressure (MAP; 153 vs. 171 mmHg for SND, 155 vs. 172 mmHg for RVLM cells). Subsequent intravenous administration of the alpha 2-adrenergic receptor agonist clonidine (5.3 micrograms/kg) produced an additional decrease in MAP (-21.2 +/- 1.9 mmHg, n = 24) and SND (-24%, n = 24), Bilateral microinjections of 8-OHDPAT into the RVLM (1 nmol/side, n = 9) or into the raphe pallidus-obscurus (2 injections of 1 nmol each, n = 7) also produced hypotension (-22.9 +/- 3.2 and -14.4 +/- 2.8 mmHg, respectively) and sympathoinhibition (-39.1 and -24.6%, respectively). Bilateral microinjection into RVLM of the alpha 2-adrenergic antagonists idazoxan (16 nmol/side, n = 6) or rauwolscine (2 nmol/side, n = 6) attenuated the sympatholytic effect of both 8-OHDPAT (13.1 micrograms/kg, iv) and clonidine (5.3 micrograms/kg iv). These results suggest that 8-OHDPAT may exert a portion of its central sympatholytic effect by activating alpha 2-adrenergic receptors in the rostroventral medulla.
Inhibition of contraction of isolated lymphatic ducts by atrial natriuretic peptide
Authors: Anderson W. D. , Kulik T. J. , Mayer J. E.
Published: December 2017

Atrial natriuretic peptide (ANP) potently relaxes blood vessels but its effect on lymphatic motility is unreported. We studied the effect of ANP, and the smooth muscle relaxing agent nitroprusside (NP), on isolated ovine mesenteric lymphatic ducts. Duct segments were mounted on a myograph, and noncumulative dose-response curves were obtained for the effect of ANP and NP on the rate and force of spontaneous (and norepinephrine-induced) duct contraction. Both ANP (threshold approximately 1 nM) and NP (threshold approximately 10 nM) in a dose-related fashion reduced the frequency and force of contraction of both spontaneously contracting and norepinephrine-stimulated duct segments. ANP may therefore affect interstitial fluid balance through its effect on lymphatic motility.
Differential baroreflex modulation of human vagal and sympathetic activity
Authors: Fritsch J. M. , Smith M. L. , Simmons D. T. , Eckberg D. L.
Published: December 2017

We compared baroreflex modulation of human vagal-cardiac and sympathetic muscle activity in healthy volunteers by measuring R-R interval and peroneal nerve responses to a profile of positive and negative (40-65 mmHg) R-wave-triggered neck pressure steps during held expiration. R-R interval responses were sigmoid. Sympathetic activity increased abruptly with 40 mmHg pressure but returned to baseline levels as this pressure was maintained. The first decremental pressure step reduced sympathetic activity to below baseline, and the next three steps inhibited activity. During the final three steps, sympathetic activity increased to baseline, and after the return of neck pressure to ambient levels sympathetic activity increased to the highest levels recorded. Our results suggest that on a second-by-second basis human vagal-cardiac responses are determined simply by the net level of baroreceptor stimulation. Sympathetic muscle responses are determined complexly by the direction of changes (rising or falling) more than absolute arterial pressure levels and importantly by inputs from both carotid and aortic baroreceptors.
Interaction of cholecystokinin-8 and pancreatic glucagon in control of food intake in dogs
Authors: Kalogeris T. J. , Reidelberger R. D. , Mendel V. E. , Solomon T. E.
Published: December 2017

Feeding responses to continuous intravenous administration of graded doses of the COOH-terminal octapeptide of cholecystokinin (CCK-8) and pancreatic glucagon, alone and in combination, were determined in dogs fasted 4 h. Low doses of glucagon (50, 500, 5,000, 6,000 pmol.kg-1.h-1) had no effect on food intake, whereas higher doses (12 and 24 nmol.kg-1.h-1) depressed intake by 50-60%. Of the CCK-8 doses administered (50 and 400 pmol.kg-1.h-1), food intake was depressed only at the higher dose (53%). This effect was blocked by glucagon (50-5,000 pmol.kg-1.h-1). Simultaneous administration of 50 or 500 pmol.kg-1.h-1 of glucagon and 50 pmol.kg-1.h-1 of CCK-8, doses currently thought to produce plasma peptide levels similar to those occurring postprandially in dogs, had no effect on food intake. These results suggest that plasma levels of CCK and glucagon after a meal are not sufficient alone or in combination to produce satiety.
Suppression of puberty in rats by exercise: effects on hormone levels and reversal with GnRH infusion
Authors: Manning J. M. , Bronson F. H.
Published: December 2017

In an effort to better understand the effects of prolonged exercise on the hypothalamic-pituitary-ovarian axis, we made a variety of comparisons between young female rats in two treatment groups: 1) prolonged exercise, in which growth and reproductive development were arrested at a peripubertal stage by requiring rats to run for long periods of time in order to obtain food; and 2) voluntary exercise, in which same-aged control rats were fed ad libitum and given free access to a running wheel. The pulsatile secretion of luteinizing hormone (LH) and growth hormone were completely suppressed by the prolonged exercise treatment. Mean levels of follicle-stimulating hormone, prolactin, and thyroid-stimulating hormone were not affected. Prolonged exercise elevated corticosterone titers, and the secretory pattern of this steroid was changed out of phase with running activity. Tissue levels of gonadotropin-releasing hormone (GnRH) in the hypothalamus and LH in the pituitary were enhanced, not suppressed, by prolonged exercise. Most importantly, pulsatile infusions of GnRH reinstated normal pubertal development and ovulation in rats still growth restricted by the prolonged exercise treatment. The results of this study indicate that the suppressive effects of prolonged exercise somehow affect the production of the hypothalamic GnRH-pulse generator signal.
Lack of osmoregulation in Aplysia brasiliana: correlation with response of neuron R15 to osphradial stimulation
Authors: Scemes E. , Salomao L. C. , McNamara J. C. , Cassola A. C.
Published: December 2017

The exposure of Aplysia brasiliana to dilute seawater (90 and 80%) caused an increase of the relative weight, which returned to the original values after a few hours. Both osmotic and chloride concentrations of the hemolymph decreased on exposure to 80 and 90% dilute seawater, and after 3-h exposure there were no differences between the hemolymph and external media osmotic and chloride concentrations. In contrast to the clear regulatory capabilities reported for A. californica, A. brasiliana cannot maintain the osmolality of its body fluid in dilute media. In A. californica, osphradial receptors and neuron R15 are apparently involved in this regulatory mechanism. Perfusion of osphradium of A. brasiliana with dilute seawater (95-80%) did not affect electrical activity of the bursting neuron R15; perfusion with 70 and 60% seawater caused a transient increase in the duration of the quiescent period. In contrast to the model established for A. californica, in A. brasiliana no relationship was found between exposure of the osphradium to dilute media and electrical activity in neuron R15, which is in accordance with the lack of an osmoregulatory mechanism in this species. Such differences may reflect inherent differences in salinity tolerance between the two species.
Pre- and postjunctional effects of some prostanoids in human isolated vas deferens
Authors: Holmquist F. , Hedlund H. , Andersson K. E.
Published: December 2017

The effects of prostaglandin (PG) E1, PGE2, the thromboxane A2 analogue U-44069, and the prostacyclin derivative iloprost were studied on isometric contractions induced by norepinephrine (NE) and by electrical field stimulation of nerves in isolated preparations of the human vas deferens. The effects of these agents on the electrically induced release of 3H from preparations preincubated with [3H]NE were also investigated. PGE1 and PGE2 inhibited the electrically induced contractions concentration dependently. U-44069 augmented the contractions without affecting baseline tension, and in preparations where the contractions had been inhibited by PGE1 or PGE2, U-44069 restored the contractions almost to starting levels. The thromboxane A2-receptor antagonist BM 13505, having no effect or inhibitory effects on electrically induced contractions, abolished the stimulatory effect of U-44069. Contractions induced by exogenous NE were augmented by U-44069, whereas PGE1 and BM 13505 were without effects. The electrically induced release of 3H was inhibited by PGE1 and PGE2 in a concentration-dependent manner, whereas U-44069 and BM 13505 increased the release of 3H. Furthermore, the inhibitory effect of PGE1 on 3H release was partly counteracted by U-44069. Iloprost had no significant effect on electrically induced contractions or on 3H release. These results suggest that, in the human vas deferens, thromboxane A2 augments contractions predominantly through a postjunctional site of action, whereas PGs of the E type have a prejunctional inhibitory effect. In addition, the pre- and post-junctional effect profiles of U-44069 and BM 13505 suggest that there may be more than one thromboxane receptor.
Central sympathoinhibition and peripheral neuronal uptake blockade after desipramine in rabbits
Authors: Eisenhofer G. , Saigusa T. , Esler M. D. , Cox H. S. , Angus J. A. , Dorward P. K.
Published: December 2017

Peripheral- and central nervous system (CNS)-mediated effects of desipramine (Des) on sympathetic nerves and the contribution of alpha 2-adrenoceptors to these effects were studied in conscious rabbits. Blood pressure, renal sympathetic nerve activity (SNA), and norepinephrine (NE) reuptake and spillover into plasma were measured before and after intracisternal (ic) or intravenous (i.v.) administration of Des. In other animals, NE spillover responses to i.v. Des were examined before and after alpha 2-adrenoceptor blockade with i.v. idazoxan. Treatment with i.v. Des blocked neuronal reuptake and decreased renal SNA but did not alter blood pressure or NE spillover. Decreased NE release by sympathetic nerves after i.v. Des was reflected by a decrease in the combined rate of NE reuptake and spillover. Treatment with ic Des (at 1.7% of the i.v. dose) decreased blood pressure and renal SNA and produced equivalent falls in NE reuptake and spillover, indicating little peripheral effect of centrally administered Des on the efficiency of neuronal reuptake. Thus Des had two distinct actions: the drug blocked neuronal reuptake by direct actions on nerve endings and reduced SNA by actions within the CNS. After ic Des, decreased SNA produced parallel falls in NE reuptake, spillover, and blood pressure. After i.v. Des, blockade of neurotransmitter reuptake increased NE concentrations at sympathoeffector junctions offsetting the fall in SNA, so that there was little change in NE spillover or blood pressure. However, after alpha 2-adrenoceptor blockade with i.v. idazoxan, NE spillover increased in response to i.v. Des. Thus the Des-induced decrease in NE release was partly mediated by an action of raised intrasynaptic NE concentrations on inhibitory alpha 2-adrenoceptors.
Prostaglandin regulation of H+ secretion in amphibian epithelia
Authors: Yorio T. , Page R. D. , Frazier L. W.
Published: December 2017

The role of prostaglandins in regulating H+ excretion in amphibian epithelia was investigated. The abdominal skin of the southern leopard frog Rana pipiens and the urinary bladder of the toad Bufo marinus were used to measure proton excretion across their mucosal surface. Prostaglandin F2 alpha (PGF2 alpha) produced a dose-dependent inhibition of H+ excretion across the frog skin. Frogs pretreated with ibuprofen (30 mg.kg-1.day-1 for 3 days) showed an enhanced proton excretion similar to that observed when frogs are placed in chronic metabolic acidosis. The number of mitochondria-rich cells, the cells responsible for proton excretion, was also increased in frog skins after chronic metabolic acidosis or ibuprofen treatment. Mezerein and the phorbol ester 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA), activators of protein kinase C (PCK), decreased H+ excretion in frog skin, whereas the inactive phorbol 4 alpha-PMA was without an effect. The inhibition of proton excretion was similar to that observed with PGF2 alpha and suggested that the effects of PGF2 alpha and activation of PKC were mediated through a common pathway. Frogs pretreated with ibuprofen not only had an enhanced proton excretion rate but also had a decrease in cytosolic PKC activity. In another amphibian tissue, the toad urinary bladder, PGE2 inhibited proton excretion at low doses but enhanced H+ excretion at higher doses. Toads maintained under chronic metabolic acidosis had enhanced proton excretion rates and also had a threefold increase in cellular PGE2 concentration, which was consistent with the observation that PGE2 enhanced proton excretion at high doses.(ABSTRACT TRUNCATED AT 250 WORDS)
Regulation of lipoprotein lipase in adipose and muscle tissues during fasting
Authors: Ladu M. J. , Kapsas H. , Palmer W. K.
Published: December 2017

The purpose of this work was to determine the relationship between lipoprotein lipase (LPL) activity and LPL mRNA in muscle and adipose tissue in fed and fasted rats. In control animals, the correlation between enzyme activity and LPL mRNA for adipose tissue, heart, soleus, fast red vastus lateralis, and fast white vastus lateralis muscle was r = +0.97. Twenty-four hours of fasting increased LPL activity 38% in heart, reduced it 59% in adipose tissue, and had no effect on activity in the three skeletal muscles analyzed. At the same time, relative LPL mRNA concentrations were reduced 25% in adipose tissue and elevated in heart, soleus, red vastus, and white vastus muscles when compared with control concentrations. Prolonging the fast to 6 days was accompanied by a 64% reduction in adipose tissue LPL activity and an increase in the activities of slow-twitch soleus (83%) and fast-twitch red vastus lateralis muscles (193%), with no enzyme activity change in heart or white vastus lateralis muscle compared with values obtained from control fed animals. LPL mRNA concentration was reduced 66% in adipose tissue, increased more than twofold in heart, soleus, and white vastus muscle, and increased threefold in red vastus muscle. Changes in relative LPL mRNA concentration in adipose tissue induced by fasting could, in part, be accounted for by the increases seen in total RNA concentration. The relationships between enzyme activity and LPL mRNA in muscle and adipose tissue were r = 0.97 and 0.77 for 1-day and 6-day fasted animals, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Arterial baroreflex inhibition by gastric distension in rats: mediation by splanchnic afferents
Authors: Nosaka S. , Murase S. , Murata K.
Published: December 2017

Arterial baroreflexes are known to be reset during activation of defense area and somatosensory receptors-afferents. Here we report that viscerosensory activation also inhibits the baroreflexes. In chloralose-urethan-anesthetized, succinylcholine-immobilized, and artificially ventilated rats, the aortic depressor nerve was electrically stimulated while propranolol was continuously infused to elicit baroreflex hypotension (BH) and baroreflex vagal bradycardia (BVB). Hydraulic distension of the stomach with warm 0.9% NaCl solution was found to suppress BVB and BH, with a threshold intraluminal pressure at times less than 5mmHg. The gastric distension also suppressed BH in atropinized rats, suggesting that inhibition involved not only cardiac but also vascular components of baroreflexes. Bilateral splanchnectomy largely attenuated the inhibition, whereas bilateral subdiaphragmatic vagotomy had little effect. Low- as well as high-frequency stimulation of the splanchnic nerve strongly suppressed both BVB and BH, whereas only low-frequency stimulation of the subdiaphragmatic vagus inhibited baroreflexes to a slight degree. In conclusion, gastric distension suppresses BVB and BH, and this inhibition is largely mediated by afferent fibers in the splanchnic nerve. Such baroreflex inhibition may be a general consequence of mechanoreceptor activation of any visceral hollow organs because the jejunum, esophagus, and urinary bladder were all found to suppress arterial baroreflexes when distended.
Sleep in diabetic rats: effects of interleukin 1
Authors: Kapas L. , Payne L. , Obal F. , Opp M. , Johannsen L. , Krueger J. M.
Published: December 2017

Previous observations indicate that both interleukin 1 beta (IL-1 beta) and insulin are involved in sleep regulation. IL-1 beta has been reported to stimulate insulin secretion, suggesting that some of the effects of IL-1 beta are mediated by insulin. The purpose of the current experiments was to study the possible role of endogenous insulin in physiological sleep regulation and in the hypnogenic effects of exogenously administered IL-1 beta. Isotonic saline or IL-1 beta (2.5 ng) was intracerebroventricularly injected into normal and streptozocin-diabetic rats at dark onset, and sleep-wake activity and brain temperature were recorded for 24 h. Blood samples were collected every 20 min during the first hour postinjection for plasma insulin measurement. In diabetic rats, rapid-eye-movement (REM) and non-REM sleep were significantly decreased during the second part of the light period on the baseline day. IL-1 beta elicited a biphasic sleep response in both normal and diabetic rats. This initial increase in non-REM sleep during the first 4 h postinjection was followed by significant sleep suppression in both groups. Brain temperature was not affected in either group. Plasma insulin concentration decreased in response to IL-1 beta in normal rats, whereas insulin was below the level of detection in the diabetic rats. These results indicate that, although sleep is disturbed in diabetic rats, pancreatic insulin might not have a decisive role in the regulation of sleep in rats, and it does not mediate the effects of IL-1 beta on sleep-wake activity.
Regulation of glomerular atrial natriuretic factor receptor subtypes by renal sympathetic nerves
Authors: De Leon H. , Garcia R.
Published: December 2017

The modulation of glomerular atrial natriuretic factor (ANF) receptors (ANF-R1 and ANF-R2) was examined in rats after unilateral (Uni-DNx), bilateral (Bil-DNx), and sham renal denervation (Sham-DNx). Glomerular ANF receptor density was higher in both left and right kidneys (1,138 +/- 73 and 952 +/- 100 fmol/mg protein, respectively) of Bil-DNx rats than in Sham-DNx animals (302 +/- 9 and 328 +/- 13 fmol/mg protein, respectively). The denervated (left) kidney from Uni-DNx rats also showed higher ANF receptor density (1,146 +/- 68 fmol/mg protein) than the contralateral untouched kidney (602 +/- 34 fmol/mg protein). Plasma ANF-(99-126) and ANF-(1-98) levels were significantly lower in the Bil-DNx group than in either Uni-DNx or Sham-DNx animals. Affinity cross-linking studies followed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and autoradiography demonstrated that both ANF-R1 and ANF-R2 receptors were upregulated in the same proportion in denervated kidneys. Guanosine 3',5'-cyclic monophosphate production by isolated glomeruli from denervated kidneys of either Bil-DNx or Uni-DNx rats was significantly higher than that of Sham-DNx controls. We conclude that renal sympathetic nerves regulate both glomerular ANF-R1 and ANF-R2-receptor subtypes.
Differential relationships among discharges of postganglionic sympathetic nerves
Authors: Kenney M. J. , Barman S. M. , Gebber G. L. , Zhong S.
Published: December 2017

The relationships among the simultaneously recorded discharges of as many as four postganglionic sympathetic nerves were studied with coherence and phase spectral analyses in baroreceptor-denervated cats. Discharges were recorded from the inferior cardiac (CN), vertebral (VN), and renal (RN) nerves. Most of the power in sympathetic nerve discharge was less than 6 Hz, and the discharges of any two nerves coherred over a frequency band generally between 0 and 15 Hz. Peak coherence occurred between 2 and 6 Hz in most cases. Our most important observations are as follows. 1) Coherence values were significantly higher in chloralose-anesthetized than in unanesthetized decerebrate cats. 2) Coherence values were higher for near ipsilateral nerves (e.g., CN and VN) than for widely separated ipsilateral nerves (e.g., CN and RN). 3) Coherence values for most pairs were higher when the nerves were located on the same side (ipsilateral nerves) rather than on opposite sides (contralateral nerves) of the body. 4) Coherence values were higher for some functionally complementary nerves (e.g., CN and RN) than for noncomplementary nerves (e.g., VN and RN). These results support the hypothesis that the central circuits responsible for the basal discharges of different postganglionic sympathetic nerves are selectively coupled.
Vasopressin and autonomic mechanisms mediate cardiovascular actions of central serotonin
Authors: Pergola P. E. , Alper R. H.
Published: December 2017

Intracerebroventricular administration of serotonin (5-HT) to conscious rats increases mean arterial pressure (MAP) and decreases heart rate. To determine the mechanisms involved, 5-HT (2.5 micrograms) was injected intracerebroventricularly into conscious rats pretreated with various neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY 53857 abolished the increase in MAP and the bradycardia elicited by 5-HT. The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a vasopressin V1 antagonist alone, but eliminated by the combined pretreatment with prazosin plus the vasopressin antagonist. In contrast, the bradycardia was eliminated by either the vasopressin V1 antagonist or chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral ventricle of conscious rats induces sympathoexcitation and the release of vasopressin, which results in an increase in MAP; 5-HT also elicits a bradycardia mediated through an interaction of the autonomic nervous system with circulating vasopressin.
Autonomic mechanisms underlying area postrema stimulation-induced cardiovascular responses in rats
Authors: Ferguson A. V. , Smith P.
Published: December 2017

Experiments were designed to examine the autonomic mechanisms underlying the decreases in blood pressure and heart rate elicited by electrical stimulation in the rat area postrema (AP). Vagotomy was found to significantly reduce the bradycardia observed in response to AP stimulation (control -123.5 +/- 23.5 beats/min; vagotomized -7 +/- 5.4 beats/min; P less than 0.001) but was without significant effect on blood pressure responses. Hexamethonium significantly reduced both heart rate (control -225.5 +/- 11.9 beats/min; hexamethonium -5.5 +/- 2.8 beats/min; P less than 0.001) and depressor (control -35.4 +/- 4.7 mmHg; hexamethonium -6.4 +/- 0.8 mmHg; P less than 0.001) responses to such stimulation, whereas combined alpha- and beta-adrenergic blockade was without effect. The muscarinic blocking agent atropine also abolished both blood pressure (control -22.0 +/- 4.3 mmHg; atropine 2.8 +/- 4.4 mmHg; P less than 0.01) and heart rate (control -187.0 +/- 41.9 beats/min; atropine 8.8 +/- 2.6 beats/min; P less than 0.01) responses to AP stimulation. These data suggest that AP stimulation influences two separate neural pathways eliciting distinct cardiovascular responses. It would appear that activation of one of these pathways results in activation of vagal efferents to the heart and thus bradycardia. A second parallel pathway influenced by AP stimulation apparently elicits depressor response through actions on cholinergic muscarinic receptors.
Normalized input impedance and arterial decay time over heart period are independent of animal size
Authors: Westerhof N. , Elzinga G.
Published: December 2017

The arterial system of mammals in the weight range from 0.6 to 70 kg is characterized by the three-element windkessel, a succinct representation of the arterial tree consisting of the parameters peripheral resistance (Rp), total arterial compliance (C), and aortic characteristic impedance (Zc). The values of these parameters in resting conditions are related to body mass (M). The time constant, or decay time (tau), of the arterial system (defining rate of decay of aortic pressure in diastole), the product of Rp and C, is also evaluated. The dependencies of the heart period (T, inverse of heart rate), and durations of ejection (Ts) and of diastole (Td) in resting conditions are also determined as a function of M. It is found that Rp = Rp0M-0.93; Zc = Zc0M-0.97; and C = C0M+1.23, where Rp0, Zc0, and C0 are proportionality constants. Zc is thus a constant fraction of Rp in all mammals. tau is related to M as tau = tau 0M+0.29; T and Td are related to M as T = T0M+0.27 and Td = Td0M+0.30, where tau 0, T0, and Td0 are proportionality constants. The duration of diastole is thus a constant fraction of T, and the ratios T/tau and Td/tau are independent of M. The findings indicate that arterial input impedance, normalized to aortic Zc and plotted as a function of frequency normalized to heart rate, is similar for all mammals. The finding that the ratio Td/tau is the same in mammals (and Ts/T and stroke volume/M are constant) explains the constancy of pulse pressure (systolic minus diastolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)
Cholecystokinin in nucleus tractus solitarii modulates tonic and phasic gastric pressure
Authors: Talman W. T. , Andreasen K. , Calvin J. , Eversmann-Johanns S.
Published: December 2017

Local excitation of neurons at the site of termination of gastric vagal afferents in the nucleus tractus solitarii (NTS) alters gastric pressure. Microinjection of one putative satiety peptide bombesin into NTS increases pressure while substance P lowers it. Therefore, we sought to determine the effects of the microinjection of cholecystokinin octapeptide (CCK-8) from micropipettes placed stereotactically into the NTS of anesthetized rats with balloons placed in the gastric antrum to sense gastric pressure waves. Sulfated CCK-8, but not nonsulfated CCK-8, produced dose-dependent decreases of gastric pressure, transient blockade of phasic waves, and subsequent dysrhythmic phasic activity. The effects were specifically related to injections into NTS and did not occur with injections given intravenously, intracisternally, or into tissue adjacent to NTS. These results support a role for CCK-8 in central regulation of not only tonic gastric pressure but also phasic activity and gastric motility.
Release of inhibitory neurotransmitters in response to anoxia in turtle brain
Authors: Nilsson G. E. , Lutz P. L.
Published: December 2017

In mammals a massive release of the excitatory neurotransmitter glutamate, occurring within a few minutes of anoxia/ischemia, is thought to be a major mediator of anoxic brain damage. In contrast to the mammalian brain, the turtle brain is exceptionally anoxia tolerant. Using intracerebral microdialysis in turtle brain striatum, we have found a large increase in the extracellular level of the inhibitory neurotransmitter gamma-aminobutyric acid during anoxia, reaching 90 times the normoxic level after 240 min, whereas no substantial release of glutamate occurred. Moreover, the inhibitory neurotransmitters/neuromodulators glycine and taurine also displayed increased extracellular levels during anoxia. Increased extracellular levels of inhibitory amino acids may be one of the hitherto elusive mechanisms that underlie the decreased activity and energy consumption characterizing the anoxic turtle brain.
Physiological consequences of NaCl ingestion by Na(+)-depleted rats
Authors: Tordoff M. G. , Fluharty S. J. , Schulkin J.
Published: December 2017

We investigated the temporal relationships between NaCl intake, gastrointestinal Na+ content, and plasma concentrations of Na+, aldosterone, and plasma renin activity (angiotensin). Rats depleted of approximately 2.2 mmol Na+ by combined dietary Na+ restriction and furosemide injection (10 mg sc) drank a preload of 1, 2, or 3 mmol 0.5 M NaCl. Intake of a test 0.5 M NaCl solution given 15, 30, 60, or 120 min later was reduced by approximately 50% of the preload content, irrespective of the interval between preload and test. At 15 min after starting to drink, 61-71% of ingested Na+ remained in the stomach, 15-18% in the small intestine, approximately 5% was calculated to be in extracellular fluid, and less than 1% was excreted. Rates of gastric and gastrointestinal clearance of Na+ were related to the quantity of NaCl ingested. Whereas gastric emptying was initially very rapid (30-61 mumol/min) and decreased with time, gastrointestinal clearance was constant (16-39 mumol/min). Drinking 3 mmol NaCl reliably reduced plasma aldosterone concentrations within 15 min and renin activity within 30 min. Drinking 1 or 2 mmol NaCl reliably reduced levels of these hormones within 30-60 min. The results describe for the first time the distribution of Na+ after Na(+)-depleted rats drink NaCl. They suggest that the rat determines the quantity of Na+ it requires within the first 15 min of ingestion and thus does not depend on signals generated by the prolonged influence of Na+ in the gastrointestinal tract or the fall in plasma concentrations of aldosterone and angiotensin.
Intravenous nutrient-induced satiety depends on feeding-related gut signals
Authors: Walls E. K. , Willing A. E. , Koopmans H. S.
Published: December 2017

To determine whether feeding-generated gut signals act in conjunction with intravenous nutrients to suppress food intake, nutrients were infused intravenously to dark-fed rats during different portions of the 12:12 h light-dark cycle. During 4-day test periods rats received 35.5-37 kcal/day of a solution containing 25% glucose-4.25% amino acids. Food intakes were reduced by 40.5 +/- 1.1 and 30.7 +/- 1.8 kcal or 110 and 87% of the calories infused in the dark (fed) phase over 8 and 12 h, respectively. When administered in the light phase while rats were fasted, 8- and 12-h infusions reduced food intake significantly less than in the dark: 21.3 +/- 1.1 and 19.6 +/- 0.7 kcal/day or only 57 and 55% of the infused calories, respectively. With 24-h infusions, as in previous studies, food intake was reduced by 24.5 +/- 2.1 kcal/day or 68% of the infused calories. These results suggest that gut signals generated by concurrent feeding act with intravenous glucose and amino acids to produce a more compensatory reduction in daily food intake.
Functional evidence for sympathetic nerve activity in conscious cervical spinal rats
Authors: Trostel K. A. , Katz S. A. , Osborn J. W.
Published: December 2017

Experiments in anesthetized animals have demonstrated sympathetic nerve activity after cervical spinal cord transection (CST), yet little evidence exists for sympathetic nerve activity in conscious spinal animals. We determined the effect of CST on mean arterial pressure (MAP), heart rate (HR), and plasma renin activity (PRA) in conscious rats. Next, we tested for the presence of functionally significant sympathetic nerve activity 24 h after CST by measuring MAP, HR, urine flow, urinary sodium excretion (UNaV), urinary potassium excretion (UKV), and PRA before and for 2 h during administration of adrenergic antagonists (propranolol + phentolamine) or vehicle. CST resulted in significant decreases in MAP (100.0 +/- 1.6 to 75.0 +/- 1.4 mmHg), HR (353 +/- 7.5 to 315 +/- 6.6 beats/min), and PRA (2.2 +/- 0.3 to 1.2 +/- 0.2 ng angiotensin I.ml-1.h-1). Subsequent adrenergic blockade resulted in a further drop in HR (-52 +/- 21 beats/min), as well as two- to threefold increases in UNaV and UKV. We conclude that CST causes an overall decrease in sympathetic drive. However, sympathetic nerve activity to the heart and kidney remains after CST and is responsible for support of HR and retention of sodium and potassium.
Alpha 1-adrenergic receptor blockade reduces afferent and efferent glomerular arteriolar resistances in SHR
Authors: Uchino K. , Nishikimi T. , Frohlich E. D.
Published: December 2017

To assess the effects of alpha 1-adrenergic receptor blockade on intrarenal hemodynamics of spontaneously hypertensive rats (SHR), terazosin (0.015 or 0.03 mg/kg body wt) or saline was injected into SHR or normotensive Wistar-Kyoto rats (WKY) (age 16-18 wk). Single-nephron glomerular filtration rate (SNGFR) and renal glomerular filtration rate were determined with [3H]inulin infusion; effective renal blood flow was measured with p-aminohippurate. Intrarenal efferent arteriolar, proximal tubular, stop-flow pressures measurements, and tubular fluid and efferent arteriolar samplings were obtained by micropuncture techniques. Terazosin reduced arterial pressure significantly in both rat strains, but only in SHR did alpha 1-inhibition decrease glomerular hydrostatic pressure (from 58.0 +/- 1.5 to 46.6 +/- 1.1 mmHg; P less than 0.05). Terazosin did not change SNGFR or single-nephron blood flow in either strain. As a result, only in SHR did efferent glomerular arteriolar resistances decrease (0.262 +/- 0.021 to 0.193 +/- 0.014 mmHg.ml-1.min; P less than 0.05). Glomerular ultrafiltration coefficient increased only in SHR (0.034 +/- 0.005 to 0.104 +/- 0.01; P less than 0.05). These results provide further support to the concept of alpha 1-adrenergic receptor hyperresponsiveness of efferent glomerular arteriolar in SHR but not WKY.
Neuropeptide regulation of feeding in dogs
Authors: Inui A. , Okita M. , Nakajima M. , Inoue T. , Sakatani N. , Oya M. , Morioka H. , Okimura Y. , Chihara K. , Baba S.
Published: December 2017

Norepinephrine and four families of neuropeptides, namely, neuropeptide Y (NPY), opioid peptides, galanin, and growth hormone-releasing factor (GRH), have been shown to stimulate feeding after central administration. Because these studies were mainly done on laboratory rats, the present study was designed to ascertain the central stimulators of feeding in dogs. We have shown that porcine and human pancreatic polypeptides (PPs), when administered into the third cerebral ventricle (intracerebroventricularly), increased food and water intake of satiated animals but that the COOH-terminal fragments [hPP-(18-36) and hPP-(23-36)] did not do so at the same molar dose (11.9 nmol). The kappa-opioid receptor agonist dynorphin (A-(1-17) also stimulated food and water intake, whereas alpha-neoendorphin and Met-enkephalin did not. These results suggest the structural specificity of PPs and dynorphin peptides for stimulating feeding. Surprisingly, neither intracerebroventricular injections of NPY and peptide YY nor intracerebroventricular pretreatment with anti-hNPY gamma-globulin modulated feeding, stressing the species differences in the feeding response to exogenous substances and the underlying physiology. Intracerebroventricular injections of norepinephrine, GRH, galanin, and pancreastatin also failed to increase food intake, although most substances tended to or did increase water intake. These results suggest that neuropeptides play a role in a species-specific way in modulating appetite regulation.