bluuebunny/crossref_metadata_2025 huggingface dataset:
Intracranial infusion of CCK-8 derivatives suppresses food intake in rats
Authors: Mori T. , Nagai K. , Nakagawa H. , Yanaihara N.
Published: December 2017

The effects of infusions for approximately 1 wk of the synthetic COOH-terminal octapeptide of cholecystokinin (CCK-8) and its derivatives, pyroglutamyl-CCK-8 (pGlu-CCK-8) and glutaryl-CCK-8 (Glt-CCK-8), into the suprachiasmatic nucleus (SCN) of the hypothalamus of male Wistar rats on their feeding behavior under 12:12 light-dark cycle were examined. Infusion of CCK-8 (0.8 pmol/h) did not change the total daily food intake but caused slight decrease in food intake during the 12-h dark period with slight increase in the 12-h light period. Infusions of pGlu-CCK-8 (0.8 pmol/h) and Glt-CCK-8 (0.8 pmol/h) markedly reduced food intake during the 12-h dark period but had little effect in the light period and thus decreased total daily food intake. The reductions in food intake during the 12-h dark period due to infusions of the CCK-8 derivatives were greater than that due to CCK-8 infusion. Body weight changes reflected changes in food intake. CCK-8 derivatives appeared to suppress both meal size and frequency at the early part of the infusion period but reduce only meal size at the later part. Histological examination showed that infusion sites in the brain were widely damaged; however, neurons in the SCN appeared to be intact. These findings suggest that CCK-8 suppresses food intake during the dark period in rats by acting on some site(s) in the brain. The results also support the possibility that CCK-8 is degraded enzymatically in the brain, whereas the two derivatives, pGlu-CCK-8 and Glt-CCK-8, are resistant to degradation.
Pressor contributions from angiotensin and vasopressin after polyethylene glycol
Authors: Gardiner S. M. , Bennett T.
Published: December 2017

Isosmotic volume depletion was induced by subcutaneous injection of 5 ml of polyethylene glycol (PEG; 20 M; 30%) in Long-Evans rats and in rats deficient in hypothalamic vasopressin (Brattleboro rats). In the PEG-treated Long-Evans rats, captopril caused a hypotension that was greater than that seen in saline-injected controls. Pretreatment with the vasopressin (V1 receptor) antagonist d(CH2)5DAVP did not, itself, cause a fall in blood pressure, but it enhanced the hypotensive effect of captopril in the PEG-treated Long-Evans rats. The PEG-treated Brattleboro rats had similar resting blood pressures to the PEG-treated Long-Evans rats, but in the former group, captopril caused a more profound and progressive hypotension than was seen in any of the present experimental regimes used in the Long-Evans rats. This suggests that, during hypovolemia induced by PEG, Brattleboro rats were either more dependent on the renin-angiotensin system for the maintenance of arterial blood pressure than were Long-Evans rats treated acutely with a vasopressin (V1) receptor antagonist or less able to recruit sympathoadrenal mechanisms to compensate for the sudden loss of the renin-angiotensin system.
Contribution of zona incerta to osmotically induced drinking in rats
Authors: Mok D. , Mogenson G. J.
Published: December 2017

Spontaneous extracellular activity was recorded from single neurons in the rostral zona incerta (ZI) of urethan-anesthetized rats. Ventricular injections of hyperosmotic saline (1 or 2 microliter of NaCl solutions with osmolarities of 0.6 or 1.2 osmol/l) and distilled water (1 or 2 microliter) at the level of the anteroventral third ventricle (AV3V) changed the firing rate of ZI neurons. By comparison, ventricular injections of osmotic solutions at the level of the dorsal third ventricle were relatively ineffective. Injections of osmotic solutions (0.2 or 0.5 microliter of 1.2 osmol/l NaCl) into the medial preoptic area (MPO) also changed the firing rate of ZI neurons, whereas control injections into the caudate putamen were ineffective. In another series of rats, injections of procaine into the region of the rostral ZI significantly reduced drinking to injections of hyperosmotic saline into the ipsi- but not the contralateral MPO. The ZI, AV3V, and MPO have previously been reported to contribute to the neural regulation of fluid intake. These findings provide additional evidence for a role of the ZI in drinking and suggest that part of the central pathway for osmotic thirst involves a projection to neurons in the ZI from osmoreceptors in the MPO.
Hepatic splanchnic function in acutely hypoxemic humans at rest
Authors: Blackmon J. R. , Rowell L. B.
Published: December 2017

Splanchnic metabolism of O2, glucose, and lactate was studied in five normal men during rest while breathing air, 10.4% O2 [arterial O2 partial pressure (PaO2) = 34.8 Torr], and in four men breathing 7.6% O2 (PaO2 = 27.0 Torr). Despite reduction in arterial O2 content to 10.7 ml/100 ml, splanchnic O2 uptake (VO2) and arteriovenous O2 difference remained constant through a fall in hepatic venous O2 content to 7.3 ml/100 ml. Hepatic release of glucose and uptake of lactate were unaffected by either moderate or severe hypoxemia. In five other men hepatic extraction efficiency, removal rate, and clearance of norepinephrine (NE) and epinephrine (E) (radioenzymatic assay) were determined, while air and 10.27% O2 were breathed, and while NE was infused over widely ranging rates (constant in a given subject). Over arterial concentrations of 1.8-17 ng/ml for NE and 0.03-0.3 ng/ml for E, splanchnic removal was closely related to arterial concentration and was unaffected by hypoxemia. NE extraction efficiency rose from 60 (control) to 94% (during infusion in normoxia and hypoxemia); E extraction efficiency remained constant at 85% under all conditions. Hepatic clearances of both NE (556-824 ml/min) and E (630-804 ml/min) were unaffected by hypoxemia. The only observed deficiency in hepatic function was a significant decrease in extraction of indocyanine green in all 10 subjects at both levels of hypoxemia.
Oxygen binding in alligator blood related to temperature, diving, and "alkaline tide"
Authors: Weber R. E. , White F. N.
Published: December 2017

Blood of Alligator mississippiensis has a relatively high O2 affinity, the half-saturation O2 tension (P50) = 24.5 Torr at pH 7.495, the arterial, normocapnic pH at 25 degrees C. Although the overall temperature sensitivity of P50 at 15, 25, and 35 degrees C and constant pH is low, the effect on P50 almost doubles when measured at the in vivo pH of each temperature (delta Happ = -24 and -47 kJ/mol, respectively). The CO2 Bohr effect (theta CO2 = -0.95) is 5.5 times greater than the fixed acid Bohr effect (theta FA), and the Haldane effect is small (approximately 0.03 pH units). The relatively high O2 affinity may ensure efficient utilization of the lung O2 reserve during breath holding and diving, whereas its pronounced in vivo temperature sensitivity may be adaptive to the high temperature quotients of the organismic O2 requirement. The large difference between theta CO2 and theta FA will favor constancy in blood O2 affinity in the face of large activity-induced increases in blood lactate and pronounced feeding-induced alkaloses. These "alkaline tides," which result from an exchange of plasma Cl- for HCO-3 across the gut wall, appear to be only slightly compensated by increased blood CO2 tensions. The results are additionally discussed in terms of allosteric modulation of hemoglobin-O2 affinity in crocodilians.
Caudolateral areas of medulla-mediating release of ACTH in cats
Authors: Bereiter D. A. , Gann D. S.
Published: December 2017

The effect of electrical stimulation of the caudolateral brain stem on plasma adrenocorticotropin (ACTH) was assessed in cats anesthetized with alpha-chloralose-urethan. To examine the influence of stimulus pattern on ACTH release, an equal number of pulses was presented in a continuous pattern and in a burst pattern at each electrode site. Stimulation of the magnocellular portion (layers 4-6) of trigeminal nucleus caudalis evoked a significant (P less than 0.01) and equal peak change in plasma ACTH after continuous pattern (+121 +/- 32 pg/ml) and after burst pattern stimuli (+126 +/- 30 pg/ml, n = 21). In contrast, stimulation of more ventromedial portions (layers 7-8) of nucleus caudalis had no significant effect on plasma ACTH. Stimulation of the trigeminal lateral cervical region the caudal extent of the A1 noradrenergic cell group, or the lateral reticular nucleus evoked significant peak increases in plasma ACTH regardless of stimulus pattern. Transient changes in arterial pressure accompanied brain stem stimulation and were not correlated with the changes in ACTH. The results indicate that stimulation of trigeminal subnucleus caudalis, a brain stem region that processes nociceptor afferent information, evokes a prompt increase in plasma ACTH. Stimulation of brain stem regions that process autonomic and cardiovascular afferent information (A1 region, lateral reticular nucleus) also facilitate ACTH release. No significant influence of stimulus pattern on brain stem-evoked ACTH release was seen. The results support the hypothesis that the influence of the central nervous system on ACTH release may be processed by parallel pathways at the caudal brain stem level.
Effects of lung volume and O2 and CO2 content on cutaneous gas exchange in frogs
Authors: Malvin G. M. , Hlastala M. P.
Published: December 2017

The effects of lung O2 and CO2 content and volume on cutaneous gas exchange and perfusion were investigated in the frog, Rana pipiens. (Ha)-anesthetized frogs were equilibrated with 9.5% Freon-22 (Fr, chlorodifluoromethane) and 1.1% Ha. Cutaneous elimination of Fr, Ha, and CO2 into a small sample chamber on the abdomen was measured with a mass spectrometer. Introducing an air mixture into the lung decreased cutaneous Fr, Ha, and CO2 elimination. Lung inflation with an O2 mixture decreased cutaneous gas elimination more than with the air mixture. Inflation with a N2 mixture had no effect. The response to lung inflation with the air mixture was not affected by adding 4.8% CO2 to the air mixture or by atropine. Voluntary lung ventilation decreased CO2 and Fr elimination. The results indicate that intrapulmonary O2 is a factor regulating skin breathing. If a change in lung volume is also a factor, it requires a concomitant change in lung O2. Intrapulmonary CO2 and cholinergic nerves are not involved in cutaneous respiration across the abdomen.
Control of atrial natriuretic factor release in conscious dogs
Authors: Verburg K. M. , Freeman R. H. , Davis J. O. , Villarreal D. , Vari R. C.
Published: December 2017

The aim of this study was to examine the changes in the concentration of plasma immunoreactive atrial natriuretic factor (iANF) that occur in response to expansion or depletion of the extracellular fluid volume in conscious dogs. The plasma iANF concentration was also measured postprandially after the ingestion of a meal containing 125 meq of sodium. Postprandial plasma iANF increased 45% (P less than 0.05) above the base-line concentration, and this increase was accompanied by a brisk natriuresis. After a low-sodium meal, however, plasma iANF and sodium excretion failed to increase. The plasma iANF concentration increased from 57 +/- 5 to 139 +/- 36 pg/ml (P less than 0.05) immediately after volume expansion with intravenous isotonic saline infusion (2.5% body wt) administered over a 30-min period; plasma iANF remained elevated at 90 +/- 14 pg/ml (P less than 0.05) for an additional 30 min before returning toward preinfusion levels. Plasma iANF decreased 45% from 78 +/- 17 to 43 +/- 7 pg/ml (P less than 0.05) in response to the administration of ethacrynic acid (2.0 mg/kg, iv bolus) that produced an estimated 15% depletion of intravascular volume. In additional experiments the infusion of synthetic alpha-human ANF at 100 and 300 ng X kg-1 X min-1 increased (P less than 0.05) both the plasma iANF concentration and the urinary excretion of iANF. This study demonstrates that the secretion of ANF is consistently influenced by changes in the extracellular fluid volume. Furthermore, the results support the concept that ANF functions to increase postprandial sodium excretion following the ingestion of a high-sodium meal.
Rat liver free cytosolic Ca2+ and glycogen phosphorylase in endotoxicosis and sepsis
Authors: Deaciuc I. V. , Spitzer J. A.
Published: December 2017

Rats were treated with Escherichia coli endotoxin (ET) either acutely or chronically or rendered septic by cecal ligation and puncture. At 6 h after ET injection, at various intervals of continuous ET infusion, and at 17-18 h after the onset of peritonitis, animals were killed and hepatocytes were isolated. Cytosolic [Ca2+] ([Ca2+]c) was measured by quin 2 during the resting state and after stimulation with epinephrine and vasopressin. Basal and epinephrine-, vasopressin- and glucagon-stimulated glycogen phosphorylase activity were also determined. In hepatocytes from acutely ET-treated rats, resting levels of [Ca2+]c were decreased 46% from 245.8 +/- 11.0 to 131.0 +/- 8.5 nM (n = 4-6, P less than 0.05). In septic rats a 39.5% decrease was noted [i.e., from 154.0 +/- 17.7 (n = 4, sham) to 93.3 +/- 91 nM (n = 5, septic, P less than 0.05)]. These decreased [Ca2+]c levels were associated with changes of glycogen phosphorylase activity in a manner suggesting a cause and effect relationship; e.g., acute ET treatment resulted in greater than 80% depression of phosphorylase a activity, whereas sepsis induced a 58% decrease in the activity of this enzyme. In ET-infused rats the resting level of [Ca2+]c and its response to hormonal stimulation were not different from hepatocytes of saline-infused rats, although glycogen phosphorylase activity was less responsive to these hormones. The effect on the enzyme's response to Ca2+-mobilizing hormones was more marked than to glucagon. This is consistent with the concept that information flow in the Ca2+-messenger system is a site of metabolic lesions produced by endotoxicosis and sepsis.
Further discussion of a model of the REM sleep oscillator
Authors: McCarley R. W. , Massaquoi S. G.
Published: December 2017

The limit cycle feature and the grounding of our model in physiology are endorsed by Daan and Beersma [Am. J. Physiol. 251 (Regulatory Integrative Comp. Physiol. 20): R1030-R1032, 1986.] as well as the fundamental postulate of the model that the latency, duration, and intensity of the first rapid-eye-movement (REM) period depends on whether the limit cycle is entered from an internal or external trajectory, and the fact that this trajectory is determined by circadian modulation of conditions at sleep onset. We describe our reasons for preferring a more explicit formulation of the sleep onset conditions than provided in our earlier “Karmal” version of this model and provide additional details of how the control of the REM-off population decline is modeled. Additional empirical evidence is cited for the continuous circadian modulation of REM cycle parameters. We emphasize that, compared with the original simple model, the present version of the model adds only one additional “free” initial condition parameter (circadian phase) that is used to model normal sleep begun at different circadian phases and the resultant variations in REM latency, duration, intensity, and period length. We present specific predictions of the model and new supporting empirical data.
Calmodulin: biochemical, physiological, and morphological effects on Schistosoma mansoni
Authors: Thompson D. P. , Chen G. Z. , Sample A. K. , Semeyn D. R. , Bennett J. L.
Published: December 2017

Results of radioimmunoassays for the Ca2+-binding protein, calmodulin, revealed that this receptor constitutes 0.53 +/- 0.12% of the total protein in adult male Schistosoma mansoni. Schistosome calmodulin purified by Ca2+-dependent hydrophobic interaction chromatography showed an apparent molecular weight of 19 kDa, and its mobility on sodium dodecyl sulfate polyacrylamide gels was influenced by the presence of Ca2+ but not the antischistosomal drug praziquantel. Calmodulin from the parasite effected a four-fold stimulation of bovine heart adenosine 3',5'-cyclic monophosphate phosphodiesterase; this process was inhibited by removal of Ca2+ with ethyleneglycol-bis(B-aminoethylether)-N,N'-tetraacetic acid but not by praziquantel. Inhibition of calmodulin-activated processes with antipsychotic compounds in vitro resulted in a number of time- and concentration-dependent changes, including inhibition of schistosome calmodulin stimulation of bovine heart phosphodiesterase, disruption and depolarization of the parasite's tegument, and positive inotropic effects on longitudinal musculature. Results of this study indicate that calmodulin is a functional component of schistosomes and suggest that the role it serves is analogous to that obtained in other eukaryotes; i.e., it is an important component of numerous processes regulated, in part, by Ca2+.
Arterial pressure ramps provoke linear increases of heart period in humans
Authors: Fritsch J. M. , Eckberg D. L. , Graves L. D. , Wallin B. G.
Published: December 2017

A variety of methods has been used experimentally to increase baroreceptor activity and provoke transient, vagally mediated cardiac slowing in humans. We studied baroreceptor-cardiac reflex physiology in eight resting volunteers by measuring R-R interval changes during and after spontaneous brief elevations of arterial pressure, preceded by bursts of muscle sympathetic nerve activity. Arterial pressure was measured with a catheter in a brachial artery, and muscle sympathetic activity was measured with a microelectrode positioned transcutaneously in a peroneal nerve. R-R intervals were related to preceding systolic pressures with linear regression analysis. When systolic pressures were correlated with R-R intervals of the next cardiac cycle, slopes (+/- SE) averaged 12.4 +/- 2.2 ms/mmHg and correlation coefficients averaged 0.81 +/- 0.09. Baroreflex slopes were inversely related to base-line systolic pressures. These results are similar to those obtained when baroreceptors are stimulated experimentally; they suggest that elevations of arterial pressure, which are preceded by bursts of muscle sympathetic activity, trigger with one heart-beat latency highly linear increases of efferent vagal-cardiac nerve activity.
Effect of autonomic agents on renin release in the turtle, Pseudemys scripta
Authors: Cipolle M. D. , Zehr J. E. , Reinhart G. A.
Published: December 2017

Experiments were conducted in the freshwater turtle, Pseudemys scripta, to study the effect of autonomic agents on the control of renin in this primitive species. The unique finding in these studies was that, unlike mammals, isoproterenol infusion fails to increase renin activity even though heart rate and arterial pressure patterns indicated that systemic responses were similar to that in mammals. On the other hand, acetylcholine (ACh) infusion resulted in a prompt threefold elevation (P less than 0.01) of renin activity. This response was blocked by propranolol but not atropine. Other experiments demonstrated that ACh elicited a prompt elevation of circulating norepinephrine and epinephrine in these turtles and led to the hypothesis that the renin response to ACh was secondary to the release of endogenous catecholamines. This hypothesis was supported by the fact that, in reserpinized turtles, ACh failed to elicit the usual renin response. Further evidence stemmed from the fact that epinephrine administration led to a prompt fourfold increase (P less than 0.01) in renin, which could be blocked by propranolol. On the other hand, phenoxybenzamine failed to block the response under identical conditions. Taken as a whole, these data suggest that in this primitive species renin activity is elevated by endogenous catecholamines even though isoproterenol, a classical beta-adrenergic agonist, is without effect. These data illustrate again the need for caution when assuming analogy when comparing responses in primitive species with that of mammals.
Function of myoglobin in oxygen consumption by isolated perfused fish hearts
Authors: Bailey J. R. , Driedzic W. R.
Published: December 2017

Myoglobin, an intracellular O2-binding protein, plays a protective role in maintaining performance of isolated fish hearts under hypoxic conditions. This study was designed to test the hypothesis that the protein contributes to O2 consumption under conditions of increased O2 demand or hypoxia. Isolated myoglobin-rich sea raven (Hemitripterus americanus) hearts and myoglobin-poor ocean pout (Macrozoarces americanus) hearts were perfused under conditions of changing partial pressure of O2 (PO2) and afterload. Sea raven hearts maintained O2 consumption and cardiac performance at low PO2 and high afterload, whereas ocean pout hearts did not. In other cases sea raven and ocean pout hearts were treated with hydroxylamine, which renders myoglobin incapable of binding O2, and subjected to changing PO2 and afterload. Sea raven hearts could not maintain O2 consumption and cardiac performance, whereas hydroxylamine treatment had no effect on O2 consumption in ocean pout hearts under these conditions. These data provide the first evidence to support the concept that myoglobin plays a role in O2 consumption of hearts.
Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii
Authors: Silver R. B. , Jackson D. C.
Published: December 2017

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
Abnormal blood pressure recovery during ganglion blockade in diabetic rats
Authors: Hebden R. A. , Bennett T. , Gardiner S. M.
Published: December 2017

The aim of the present study was to determine the extent to which vasopressin or the renin-angiotensin system contributed to the recovery of blood pressure following acute hypotension induced by treatment with pentolinium and captopril, or pentolinium and the vasopressin antagonist d(CH2)5DAVP, respectively, in conscious, free-moving rats treated 21 days previously with saline or streptozotocin (STZ) (60 mg/kg ip). Half the animals given STZ were subsequently treated with insulin (about 4.5 U/day). The STZ-treated animals demonstrated a resting bradycardia and systolic hypotension. The vasopressin-mediated recovery in blood pressure seen following administration of pentolinium, in the presence of captopril, and the renin-angiotensin-mediated recovery seen following administration of pentolinium, in the presence of d(CH2)5DAVP, were both found to be significantly (P less than 0.05) attenuated in the STZ-treated animals. These abnormalities were absent in the animals injected with STZ and treated daily with insulin, but receiving their last dose 24 h before measurement. At that time the animals had elevated blood glucoses. These results indicate that the abnormalities observed were not due to toxic effects of STZ or to hyperglycemia per se.
Factors from paraventricular nucleus mediating adrenocorticotropin release in cats
Authors: Carlson D. E. , Gann D. S.
Published: December 2017

Experiments were conducted in alpha-chloralose-urethan-anesthetized cats. We stimulated the hypothalamic paraventricular nucleus (PVH) electrically before and after intracerebroventricular (icv) injection of an antiserum to arginine vasopressin (AVP), one to corticotropin-releasing factor (CRF), or one to normal rabbit serum (NRS). Stimulation of the ventral portion of the dorsal PVH led to increases in arterial pressure and heart rate that did not change after any of the icv treatments. However, the effect of each agent on the increases in plasma adrenocorticotropin (ACTH) after stimulation was related to the area of the PVH that was stimulated. The response to stimulation of a rostral area that extended dorsally from the anterior PVH was blocked completely by the anti-AVP but not by anti-CRF or NRS. The response to stimulation of a caudal area located in the dorsal PVH was attenuated after anti-CRF, unchanged after anti-AVP, and augmented after NRS. The antibodies that were given icv were found immunocytochemically to enter the median eminence at sites that include some adjacent to the portal vessels. Immunocytochemical localization of AVP- and of CRF-containing neurons in the PVH showed that the anterior PVH had the highest proportion of AVP neurons in the PVH but had only a few CRF neurons. In contrast, the dorsal PVH contained the highest density of CRF neurons in the PVH as well as some AVP neurons. We suggest that, in the cat, the primary releasing factor for the anterior PVH is AVP and that for the dorsal PVH is CRF.
Sweat secretion by human axillary apoeccrine sweat gland in vitro
Authors: Sato K. , Sato F.
Published: December 2017

Functional characteristics of isolated single human axillary apoeccrine sweat glands have been studied using in vitro sweat induction methods. Sustained copious clear fluid secretion was evoked by methacholine (MCh), epinephrine (EP), isoproterenol (ISO), and phenylephrine (PL) in decreasing order in a pharmacologically specific manner. Apoeccrine glands showed a higher cholinergic sensitivity than eccrine sweat glands, as shown by the apparent association constant for MCh of 2.7 X 10(-7) M compared with 2.1 X 10(-6) M for the axillary eccrine sweat gland. The average total sweat rate of the apoeccrine gland for a 30-min period was sevenfold higher than that of the eccrine sweat gland. In contrast, isolated apocrine glands showed intermittent pulsatile turbid sweat secretion in response to MCh or EP. The Na+ and K+ concentration of apoeccrine glands was nearly isotonic, whereas those of apocrine sweat was 120-140 mM for Na+ and 10-20 mM for K+. Apoeccrine ductal Na+ absorption was also observed in the apoeccrine glands and was no more efficient than that of the axillary eccrine sweat gland. Thus apoeccrine sweat glands are functionally and pharmacologically distinct from axillary apocrine glands and significantly contribute to overall axillary sweating in humans.
Pressoreceptor modulation of renal but not splenic sympathetic reflexes
Authors: Tobey J. C. , Weaver L. C.
Published: December 2017

Influences of sinoaortic and vagally innervated vascular pressoreceptors on excitatory splenic and renal sympathetic responses to splenic receptor stimulation were investigated in anesthetized cats. These experiments demonstrated that these pressoreceptors have little apparent effect on the magnitude of splenic nerve responses to splenic receptor stimulation by capsaicin, bradykinin, or congestion. In contrast, activation of these pressoreceptors attenuated renal nerve responses to splenic receptor stimulation. Influences of sinoaortic and vagally innervated receptors on tonic sympathetic nerve activity also were evaluated. Stimulation of these receptors by small increases in arterial pressure (15–21 mmHg) caused equivalent inhibition of splenic and renal nerve activity; large increases (50–66 mmHg) caused significantly greater inhibition of renal than splenic nerve activity. These results illustrate that excitatory renal and splenic sympathetic responses to splenic receptor stimulation are not suppressed equally by pressoreceptor activation, vascular pressoreceptors can have greater inhibitory influences on tonic renal than splenic nerve activity, and vascular pressoreceptor influences on sympathetic reflexes are similar to those on tonic nerve activity.
Sulfate transport by chick renal tubule brush-border and basolateral membranes
Authors: Renfro J. L. , Clark N. B. , Metts R. E. , Lynch M. A.
Published: December 2017

Brush-border and basolateral membrane vesicles (BBMV and BLMV, respectively) were prepared from chick kidney by a calcium precipitation method and by centrifugation on an 8% Percoll self-generating gradient, respectively. In BBMV a 100-mM Na gluconate gradient, out greater than in, caused concentrative sulfate uptake approximately fivefold greater at 1 min than at 60 min (equilibrium) whether or not the membranes were short-circuited with 100 mM K gluconate, in = out, plus 20 micrograms valinomycin/mg protein. A 48-mM HCO3- gradient, in greater than out, stimulated a 2.5-fold higher uptake at 1 min than at 60 min, and short circuiting as above had no effect on the magnitude of this response. Imposition of a H+ gradient (pH 5.4 out vs. pH 7.4 in) caused concentrative uptake fourfold higher at 1 min than at equilibrium. Short circuiting as above or addition of 0.1 mM carbonyl cyanide m-chlorophenylhydrazone (CCCP) significantly inhibited the pH gradient effect. Creation of an inside positive electrical potential with 100 mM K gluconate, out greater than in, plus valinomycin, also caused concentrative sulfate uptake. The K gradient in the absence of valinomycin had no effect on sulfate uptake (compared with isosmotic mannitol). Based on inhibitor/competitor effects, these are distinct sulfate transport processes. In chick BLMV, imposition of an HCO3- gradient, in greater than out, produced concentrative sulfate uptake; however, neither Na+ nor H+ gradients had significant effects at 15 s. 4-Acetamido-4'-isothiocyanostilbene 2,2–-disulfonic acid disodium at 0.1 mM was an effective inhibitor of BLMV bicarbonate-sulfate exchange; however, neither Cl-, SCN-, nor CCCP inhibited.
Hepatic function in rats after spaceflight: effects on lipids, glycogen, and enzymes
Authors: Merrill A. H. , Wang E. , Jones D. P. , Hargrove J. L.
Published: December 2017

The inclusion of rats aboard Spacelab 3 (SL-3) allowed analyses of liver lipids, glycogen, hepatic enzymes of cholesterol, glycerolipid and sphingolipid biosynthesis, and other enzyme activities. Glycogen content was markedly elevated in livers from the flight animals compared with controls. Cholesterol was 24% (P less than 0.04) lower in livers from the experimental groups, whereas blood cholesterol was 19% higher (P less than 0.05). The activity of 3-hydroxy-3-methylglutaryl-CoA reductase, the rate-limiting enzyme of steroid biosynthesis, was 80% lower (P less than 0.01). Total phospholipids and sphingolipid levels did not differ significantly. The specific activity of fatty acyl-CoA synthetase, which is responsible for activation of fatty acids, was 37% (P less than 0.05) higher in microsomes from the rats on SL-3; however, since these animals had 25% less microsomal protein (P less than 0.02), there was no difference per gram of liver. The initial enzymes of sphingolipid and glycerolipid biosynthesis were assayed; serine palmitoyltransferase was 40% lower (P less than 0.01), and glycerol 3-phosphate acyltransferase did not differ. Hepatic cytochrome P-450 content decreased by 50% after spaceflight. Enzymes that did not differ significantly between the two groups include cytochrome b5, glutathione S-transferase, tyrosine aminotransferase, aspartate aminotransferase, and cystathionase. These findings suggest that spaceflight alters hepatic metabolism of several classes of compounds.
Separation of captopril effects on salt and water intake by subfornical organ lesions
Authors: Thunhorst R. L. , Fitts D. A. , Simpson J. B.
Published: December 2017

Several experiments tested whether the subfornical organ (SFO) is necessary for water or NaCl intake arising from angiotensin-converting enzyme (CE) blockade with captopril (CAP) in the drinking fluids (0.1 mg/ml). Peripheral CAP was given to rats acutely following 24-h water deprivation or chronically over several days, either with water alone available for drinking or with 0.3 M NaCl in choice with water. Control rats drank more water, and NaCl when it was available, during CAP treatment, whereas rats with SFO damage increased NaCl intake only. CAP decreased urinary volume (UV) and increased urinary potassium excretion (UKV) during rehydration with only water available and increased urinary sodium excretion (UNaV) with NaCl present. Regardless of CAP treatment, rats with SFO damage had increased electrolyte concentrations and excretions during rehydration with only water available and increased UK with NaCl present, compared with controls. Oral CAP did not have an aversive taste at the dose used here. We conclude that the SFO is necessary for CAP-enhanced water, but not NaCl, intake and suggest that different neurological mechanisms control ingestion of each fluid during CAP.
Secretory activity in salt glands of birds and turtles: stimulation via cyclic AMP
Authors: Shuttleworth T. J. , Thompson J. L.
Published: December 2017

O2 consumption in tissue slices from the nasal salt gland of the duck and the lachrymal salt gland of Malaclemys is stimulated by methacholine, a stimulation that is inhibited by bumetanide and by ouabain. In addition, the calcium ionophore A23187 mimics the action of methacholine in stimulating this secretion-related O2 consumption in both glands, suggesting a second-messenger role for this ion in the cholinergic response. However, the adenylate cyclase activator, forskolin, and the cyclic AMP analogue, 8-cpt-cAMP, also stimulate ouabain-sensitive and bumetanide-sensitive O2 consumption in both the duck gland and the Malaclemys gland. It is suggested that the mechanism of salt secretion in the Malaclemys lachrymal gland conforms to that previously described for other extrarenal salt-secreting tissues in nonmammalian vertebrates and, as in the bird gland, is subject to a cholinergic regulation potentially acting via changes in intracellular calcium. In addition to this, secretory activity in both the avian and the turtle glands can be stimulated by a previously undisclosed adenylate cyclase-cyclic AMP system. The identity of the primary signal for such a system is not known, nor is the nature of any interrelationship between the two second-messenger systems that have been identified in these glands.
Effects of hypercapnia on variability of normal respiratory behavior in awake cats
Authors: Szlyk P. C. , Jennings D. B.
Published: December 2017

Resting quiet awake cats breathing air in a steady state have a range of respiratory behavior, and this encompasses nonpurring and purring (D. B. Jennings and P. C. Szlyk, Can. J. Physiol. Pharmacol. 63: 148-154, 1985). On a given study day, individual cats usually breathed in a limited part of their potential respiratory range. Respiratory pattern, such as average breath frequency (f) and average tidal volume (VT) utilized for a given level of ventilation (V), could be predicted when cats breathed air; as well, inspiratory (TI) and expiratory (TE) times were specific for a given breath f. Inhalation of 2% and 4% CO2 in air caused an average increase in ventilation of 16 and 100%, respectively but breath-to-breath variability of V, f, and VT persisted at each fractional concentration of inspired CO2 (FICO2). The range of different V utilized breath to breath when breathing 2% CO2 overlapped with V during air control studies. Substantial overlap with control V also occurred in three of six cats when breathing 4% CO2. The most consistent effect of progressive hypercapnia was to increase VT and decrease f at a given level of V; increase in V during hypercapnia was accounted for by an increase in mean inspiratory flow (VT/TI). Hypercapnia also caused the fraction of breathing cycle devoted to inspiration (TI/TT) to increase at low f but not at high f.
Attenuated sodium appetite in response to sodium deficiency in Fischer-344 rats
Authors: Midkiff E. E. , Fitts D. A. , Simpson J. B. , Bernstein I. L.
Published: December 2017

Fischer-344 (F-344) rats avoid NaCl solutions which are preferred by other strains. The present studies examined Na appetite induced by two methods: maintenance on a Na-deficient diet, and Na depletion by injection of furosemide. In comparison with outbred Wistar rats, F-344 rats showed no evidence of Na appetite induced by Na-deficient diet after the first 15 min (study 1) and demonstrated attenuated Na appetite in response to the natriuretic effects of furosemide (study 2). Since Na loss by Wistar and F-344 rats was similar, it is likely that this reduced Na appetite was due to hedonic differences between the strains rather than to differential renal response to furosemide or Na-deficient diet.
Guinea pig lung development: antioxidant enzymes and premature survival in high O2
Authors: Sosenko I. R. , Frank L.
Published: December 2017

Whereas guinea pigs have advanced prenatal morphological lung development, their surfactant development is not "precocious" compared with other small laboratory animals. To investigate whether maturation of the antioxidant enzyme (AOE) system coincides more closely with surfactant development or with morphological maturation, we assayed fetal guinea pig lungs at gestational days 49-69 for superoxide dismutase, catalase, and glutathione peroxidase activities. We found that elevations in pulmonary AOE occurred in parallel with increases in surfactant during the final 10-15% of gestation. Since newborn guinea pigs behave more like adult animals in their relative intolerance to hyperoxia, we explored whether prematurely delivered guinea pigs would tolerate high O2 exposure better than full-term newborns. We found that prematures have markedly improved hyperoxic tolerance compared with newborns (time at which 50% of animals died in greater than 95% O2, 6.4 days vs. 4.5 days, respectively, P less than 0.05); and (unlike newborns) premature pups are capable of mounting an elevated AOE response to hyperoxic challenge. Thus premature guinea pigs behave more like full-term newborns of other species in respect to hyperoxic tolerance, an additional precocious feature of guinea pig development.
Normalization of hemodynamic parameters: application to vascular resistance and impedance
Authors: Liu Z. R. , Yin F. C.
Published: December 2017

Comparison of hemodynamic parameters among different species is complicated by the wide variety of body sizes and shapes. Although some parameters such as blood pressure and flow velocity seem to have similar absolute values among species, most other parameters such as cardiac output, pulse wave velocity, and heart rate vary greatly. Comparisons would be facilitated if one uses indices that are independent of body size and/or shape. An ideal index will bring values for individuals or species of different sizes into the same range and yet exhibit large relative changes to responses to small increments of an intervention in an individual. In this paper we demonstrate how dimensional analysis together with Buckingham's pi theorem and the assumption of biological similarity can be used to derive dimensionless hemodynamic normalization indices. Using data from the literature and from our own laboratory, we illustrate the approach by examining resistance and impedance. We compare our results with previously proposed methods of accounting for different body sizes, namely, dividing impedance by resistance or vice versa, multiplying by body weight, and using flow velocity rather than volume flow in the calculations. Both of our proposed indices bring the values for arterial and pulmonary resistance and impedance for rats, rabbits, dogs, and humans into the same range, although the variability among species using our indices is twice that of those previously proposed. On the other hand, the relative changes of our two indices induced by vasoactive agents or exercise in a dog are from two to five times greater than either the absolute values themselves or the previously used indices.
Vasopressin release in response to nausea-producing agents and cholecystokinin in monkeys
Authors: Verbalis J. G. , Richardson D. W. , Stricker E. M.
Published: December 2017

Administration of lithium chloride and copper sulfate to adult monkeys caused marked elevations in plasma vasopressin (AVP) levels without significant increases in plasma oxytocin (OT) levels. Emesis was produced in five of the seven animals given these agents, in support of nausea as the main stimulus to AVP release. A similar pattern of AVP release without OT release was found after administration of cholecystokinin (CCK). Although most monkeys vomited in response to 10 micrograms/kg of CCK, a significant increase in plasma AVP levels also was produced with a dose of 1 microgram/kg, which did not produce emesis in any animal. These findings are in marked contrast with previous results in rats, which indicated that lithium chloride, copper sulfate, and CCK each stimulated OT rather than AVP release. Despite this interspecies difference, the significant neurohypophysial hormone secretion in response to both nausea-producing agents and CCK suggests that AVP secretion in monkeys, similar to OT secretion in rats, might reflect activation of central pathways mediating nausea and/or inhibition of food intake, even when overt illness is not produced.
Pressor action of intravenous angiotensin II reduces drinking response in rats
Authors: Robinson M. M. , Evered M. D.
Published: December 2017

We investigated whether the pressor response to intravenous angiotensin II (ANG II) suppresses drinking. All experiments were done on conscious water-replete rats (200-400 g) with chronic vascular cannulas. Two rates of ANG II infusion (16.7 and 100 ng/min for 90 min) were tested; captopril (0.33 mg/min) was infused simultaneously to prevent endogenous production of ANG II. Both doses of ANG II increased mean arterial pressure (MAP) by 40-50 mmHg for the duration of the infusions, but water intakes were small. The drinking response was increased as much as fivefold, however, when the pressor response was reduced by injecting either isoproterenol (0.01 or 0.1 mg/kg, sc), diazoxide (20, 30, or 75 mg/kg, sc), or minoxidil (10 mg/kg, ip) 15 min after starting the ANG II infusion. The closer MAP was returned to normal, the greater was the drinking response. Since lowering MAP also reduced urinary water losses, net fluid intake increased even more dramatically. It is unlikely that the vasodilators directly stimulated thirst in the experiments because the dose of captopril used completely blocked drinking to these agents given alone. A situation of high circulating levels of ANG II but with MAP near or below normal more closely resembles physiological conditions of dehydration. Our results demonstrate that intravenous ANG II is a very potent dipsogen under these conditions.
Renal nerves mediate blunted natriuresis to atrial natriuretic peptide in cirrhotic rats
Authors: Koepke J. P. , Jones S. , DiBona G. F.
Published: December 2017

The diuretic and natriuretic responses to atrial natriuretic peptide in conscious rats with cirrhosis (chronic bile duct ligation) were examined. Cirrhotic rats had sodium retention, ascites, and elevated liver weights. In conscious control rats, atrial natriuretic peptide increased urine flow rate and urinary sodium excretion. In conscious cirrhotic rats, atrial natriuretic peptide had no effect on urine flow rate or urinary sodium excretion. Renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide in cirrhotic rats. Renal sympathetic nerve activity increased in conscious cirrhotic rats during infusion of atrial natriuretic peptide but decreased in conscious control rats. Inhibition of the renin-angiotensin system with captopril had no effect on the diuretic or natriuretic responses to atrial natriuretic peptide in conscious control or cirrhotic rats. Mean arterial pressure, glomerular filtration rate, and renal plasma flow were affected similarly by atrial natriuretic peptide in control and cirrhotic rats. Increased renal sympathetic nerve activity, but not angiotensin II, mediates the blunted diuretic and natriuretic responses to atrial natriuretic peptide in conscious cirrhotic rats.
Renal function and sodium balance in conscious Dahl S and R rats
Authors: Roman R. J. , Osborn J. L.
Published: December 2017

Renal transplantation studies have indicated that some form of renal dysfunction underlies the development of hypertension in Dahl salt-sensitive (S) rats. In the present study, we compared renal hemodynamic and tubular function of conscious Dahl S and salt-resistant (R) rats. Prehypertensive Dahl S rats had a blunted natriuretic response to an intravenous isotonic sodium chloride load compared with the responses of normotensive Dahl R or hypertensive Dahl S rats. This difference was probably not related to a generalized defect in renal tubular handling of sodium and water, since prehypertensive Dahl S rats excreted quantities of sodium comparable to those of R or hypertensive S rats when infused with hypertonic sodium chloride solutions. Dahl S rats also elevated free water clearance and lowered urine osmolality similar to R rats when challenged with a hypotonic saline load. Renal blood flows and glomerular filtration rates were similar in prehypertensive Dahl S, hypertensive Dahl S, and Dahl R rats. The possible link between sodium retention and the development of hypertension in Dahl S rats was examined further by measuring the changes in sodium and water balance, extracellular fluid volume (ECV), and blood pressure after exposure to an 8% sodium chloride diet. No differences could be detected in the salt and water balances of Dahl S and R rats exposed to a high-salt diet for 14 days. ECV increased significantly by 10% in Dahl S rats on the 1st day of a high-salt diet, whereas no change was observed in Dahl R animals.(ABSTRACT TRUNCATED AT 250 WORDS)
Angiotensin II infusion increases thoracic duct lymph flow in chronically catheterized sheep
Authors: Valenzuela G. J. , Hewitt C. W. , Graham A. D.
Published: December 2017

Both pregnancy and estrogen administration are associated with a decrease in the systemic vasculature pressor response to angiotensin II infusion; however, the lymphatic vessel system response is not clear. In the present study we infused angiotensin II to nine nonpregnant splenectomized ewes with 0.1, 10, or 1,000 ng X kg-1 X min-1 for a 5-min period at each dose. At the lowest dose the mean arterial pressure increased from 10 to 20% over base line. At the highest dose, the left thoracic duct flow rate peaked at 361% 10 min after the infusion was started, whereas arterial pressure peaked at 183% of the control value. Peak lymph flow occurred 4-6 min after the maximal increase in mean systemic arterial pressure. Neither hematocrit nor venous pressure were altered at any of the doses administered. This suggests that the interstitial fluid space pressure remained unchanged and that the increase in lymph flow was not secondary to fluid transfer from the intravascular system. We postulate, therefore, that the effect of angiotensin II in the increase of lymph flow rate is by direct action on the lymphatic vessels themselves.