bluuebunny/crossref_metadata_2025 huggingface dataset:
Alterations in cellular Ca2+ regulation in the liver in endotoxic shock
Authors: Sayeed M. M.
Published: December 2017

Effects of Salmonella enteritidis endotoxin on cellular Ca2+ regulation were studied in the liver. Rats were given intravenous injections of saline (control) or endotoxin (15 mg/kg). They were killed 5 h later, at which time endotoxin-injected rats showed signs of shock. Liver slices were used to measure Ca2+ efflux from the intracellular Ca2+ pool and the size of that pool. 45Ca uptake was measured in isolated endoplasmic reticulum (ER) from livers. 45Ca efflux and uptake were also measured in control liver slices and ER in the presence of endotoxin (250 micrograms/ml) in vitro. In control livers, 45Ca efflux from the intracellular pool was sensitive to iodoacetate and 45Ca uptake by ER was ATP dependent. These active Ca2+ movements were significantly attenuated by endotoxin in vitro but were unaltered in livers of endotoxic rats. However, the intracellular Ca2+ pool size and norepinephrine (NE) regulation of cellular Ca2+ were adversely affected in endotoxic shock. Though the application of 1 microM NE to control liver slices significantly stimulated 45Ca efflux, it failed to stimulate efflux in liver slices of endotoxic rats. The intracellular Ca2+ pool in endotoxic livers (mean +/- SE = 553 +/- 23 mumol/kg tissue) was significantly larger than in controls (413 +/- 17). These results suggest that during endotoxic shock there is a depletion of the NE-mobilized activator Ca2+ in liver that could lead to a failure of alpha-adrenergic stimulation of hepatic glucose production. The increased sequestration of Ca2+ in the intracellular pool in endotoxic rat liver cells could be due to an influx of extracellular Ca2+ and may predispose these cells to Ca2+ overload.
Atrial stretch increases sodium excretion independently of release of atrial peptides
Authors: Goetz K. L. , Wang B. C. , Geer P. G. , Leadley R. J. , Reinhardt H. W.
Published: December 2017

The effects of atrial distension on plasma atrial natriuretic factor and renal salt and water excretion were studied in normal dogs and in cardiac-denervated dogs. In five conscious normal dogs, elevation of left atrial pressure (7.8 Torr) consistently increased plasma concentrations of radioimmunoassayable atrial natriuretic factor (riANF), urine flow, and sodium excretion. Elevation of right atrial pressure (3.5 Torr) in the same five dogs also consistently increased riANF, but sodium excretion and urine flow did not increase. In four conscious cardiac-denervated dogs, elevation of left atrial pressure (9.2 Torr) consistently increased riANF, but urine flow and sodium excretion did not increase. Because atrial distension increased plasma riANF in each of the three types of experiments, but urine flow and sodium excretion increased in only one type, we conclude that atrial natriuretic peptides are not responsible for the diuretic and natriuretic responses elicited by left atrial distension. It is conceivable, of course, that atrial peptides released during atrial distension may act synergistically with other changes evoked by atrial distension and thereby contribute to the natriuresis elicited by left atrial stretch. However, the increase in plasma riANF during atrial distension appears to be incapable of independently increasing salt and water excretion in the conscious dog.
Reduced osmotic and nonosmotic release of vasopressin after meclofenamate in the conscious dog
Authors: Walker B. R. , Erickson A. L. , Arnold P. E. , Burke T. J. , Berl T.
Published: December 2017

Both in vivo as well as in vitro experiments suggest that prostaglandins (PG) may influence arginine vasopressin (AVP) release. Recent studies on conscious dogs have shown that cyclooxygenase inhibition with meclofenamate reduces basal AVP release as well as AVP release in response to hypoxia. The current experiments were performed in order to test whether PG synthesis inhibition affects osmotic- and nonosmotic-stimulated AVP release in a similar manner. Osmotic AVP release was tested by slowly infusing hypertonic saline intravenously in water-diuresing dogs and serially sampling plasma for AVP concentration. Experiments were performed both with and without meclofenamate (2 mg/kg and 2 mg X kg-1 X h-1 iv) pretreatment. AVP release to a comparable osmotic stimulus was greatly reduced after meclofenamate administration. Nonosmotic AVP release was tested by inducing systemic hypotension with an intravenous infusion of nitroprusside. Hypotension was associated with an increase in AVP concentration, which was partially blunted after meclofenamate administration. Experiments performed with only a saline vehicle administered showed no decrease in AVP release in response to comparable hypotension. The findings of these studies suggest that endogenous PG may be involved in both osmotic and nonosmotic AVP release in the conscious dog.
Mechanical effects of vasoactive drugs on carotid sinus
Authors: Bell L. B. , Seagard J. L. , Zuperku E. J. , Kampine J. P.
Published: December 2017

Carotid sinus diameter (CSD) is influenced by changes in sympathetic tone and vasoactive agents. This study was designed to determine which mechanical properties of the carotid sinus region were influenced by infusing vasoconstrictors (epinephrine, 4.56 X 10(-6) M, and phenylephrine, 9.85 X 10(-5) M) and a vasodilator (nitroprusside, 1.68 X 10(-4) M). CSD, carotid sinus length (CSL), pressure (CSP), and compliance (CSC), and arterial pressure were all recorded simultaneously from the isolated constant-flow-perfused carotid sinus region of 11 anesthetized dogs (35 mg/kg pentobarbital sodium) before and after drug perfusion. CSC was measured by a method previously described in which 13 microliters of perfusate is injected into the segment in a step-like manner and the resultant step change in pressure recorded. The compliance of the vessel segment is read on-line after a calibration procedure. CSD and CSL were measured using sonomicrometer length gauges positioned across and along the length of the carotid sinus segment. At a CSP of 99.9 +/- 0.6 (SE) mmHg, CSD, CSL, and CSC were 8.50 +/- 0.44 mm, 9.44 +/- 0.84 mm, and 0.46 +/- 0.05 microliter/mmHg, respectively. Decreasing CSP to 50 mmHg significantly reduced CSD and CSL and increased CSC. Increasing CSP to 150 mmHg produced opposite results. Vasoconstrictor drug infusion significantly decreased and vasodilator drug infusion significantly increased both CSD and CSL, producing parallel shifts in the CSP-CSD and -CSL curves toward and away from the pressure axis. The shift to new pressure-volume curves resulted in no change in CSC in response to the vasoactive agents.
Uteroplacental O2 uptake: continuous measurements during uterine quiescence and contractions
Authors: Longo L. D. , Dale P. S. , Gilbert R. D.
Published: December 2017

To determine the constancy of uteroplacental O2 uptake (VO2) during uterine quiescence and both spontaneous and oxytocin-induced uterine contractions, we have developed a method to measure VO2 continuously and reproducibly. In seven ewes during uterine quiescence, total uterine blood flow (Qut) averaged 200 ml X min-1 X kg uterine contents-1, with intra-animal SD of 18 min X min-1 X kg-1 and interanimal SD of 86 ml X min-1 X kg-1. Uterine arteriovenous O2 content difference averaged 4.2 +/- 0.5 ml X dl-1. VO2 averaged 8.2 +/- 1.2 ml X min-1 X kg-1, with interanimal SD of 3.6 ml X min-1 X kg-1. During 21 spontaneous prelabor contractions, VO2 decreased 3.8% to 8.7 +/- 0.3 ml X min-1 X kg-1 (NS) during the contraction and subsequently increased 12.3% to 10.1 +/- 0.3 ml X min-1 X kg-1 (P less than 0.05) near the end of the contraction. With oxytocin-induced contractions, VO2 fell 10% to 6.4 +/- 0.2 ml X min-1 X kg-1 at the contraction onset (P less than 0.05) but by the end of the contraction had increased 6.1% to 7.6 +/- 0.2 ml X min-1 X kg-1 (NS). In conclusion, uteroplacental VO2 was measured continuously and reproducibly using relatively straightforward methodology; uteroplacental blood flow, arteriovenous O2 content difference, and uteroplacental O2 uptake were normally distributed with coefficients of variation less than 15%; and during both spontaneous and oxytocin-induced uterine contractions Qut decreased significantly, while VO2 initially decreased moderately and then showed an overshoot, during the contraction.
Effect of relative shell size in turtles on water and electrolyte composition
Authors: Dunson W. A. , Heatwole H.
Published: December 2017

Interspecific differences in water, sodium, and potassium concentrations of entire freshwater turtles are related to the relative size of the shell. Species with proportionately smaller shells have higher water and potassium concentrations but lower sodium concentrations (expressed as mumol/g wet mass). These effects are associated with variation in the amount of shell bone, which is lower in water and potassium concentrations than other tissues. Within a single species there are also differences in composition related to total wet mass and relative shell mass. Smaller turtles have a relatively larger overall water concentration, a lower overall sodium concentration (expressed as mumol/g wet mass), and a larger relative wet mass of shell (expressed as % total wet mass). The shell in small turtles is lower in relative dry mass, higher in water concentration, and lower in sodium concentration (expressed as mumol/g wet mass) than in large turtles. There is also a striking inverse size-related difference in the proportion of overall sodium that is exchangeable. This is due to a decrease in the proportion of exchangeable sodium in the shell of larger turtles, perhaps related to progressive calcification. The magnitude of the effects of size and/or age on water and electrolyte composition of turtles has not been previously recognized but must now be taken into account before any interspecific or intraspecific comparisons in body composition are made.
Control of sodium excretion by angiotensin II: intrarenal mechanisms and blood pressure regulation
Authors: Hall J. E.
Published: December 2017

Angiotensin II (ANG II) is one of the body's most powerful regulators of Na excretion, operating through extrarenal mechanisms, such as stimulation of aldosterone secretion, as well as intrarenal mechanisms. Considerable evidence suggests that the intrarenal actions of ANG II are quantitatively more important than changes in aldosterone secretion in the normal day-to-day regulation of Na balance and arterial pressure. ANG II at physiological concentrations increases proximal tubular reabsorption, but further studies are needed to determine whether ANG II also has an important effect on more distal tubular segments. ANG II also markedly constricts efferent arterioles, tending to increase Na reabsorption by altering peritubular capillary physical forces and also helping to prevent excessive decreases in glomerular filtration rate. ANG II may also decrease Na excretion and increase urine concentrating ability by reducing renal medullary blood flow. Regulation of Na excretion by ANG II is closely linked with arterial pressure control and volume homeostasis through the renal pressure natriuresis mechanism. Under many physiological conditions, such as changes in Na intake, ANG II greatly multiplies the effectiveness of the pressure natriuresis mechanism to prevent fluctuations in body fluid volume and arterial pressure. In circumstances associated with circulatory depression, such as decreased cardiac function, reductions in blood pressure and increased ANG II formation cause Na retention until arterial pressure is restored to normal. However, in pathophysiological conditions in which ANG II is inappropriately elevated, increased arterial pressure (hypertension) is required for the kidney to "escape" the potent antinatriuretic actions of ANG II and to return Na excretion to normal via the pressure natriuresis mechanism.
Differential effect of behavior on cardiac and vasomotor baroreflex responses
Authors: Combs C. A. , Smith O. A. , Astley C. A. , Feigl E. O.
Published: December 2017

Bilateral carotid occlusion was performed in seven baboons during dynamic leg exercise, static arm exercise, feeding, rest, and sleep. The baroreceptor reflex effects on blood pressure, heart rate and interval, renal blood flow, and terminal aortic blood flow were determined during each behavior. The carotid sinus baroreflex increase in blood pressure and heart rate was greatest during sleep and least during exercise. The hindlimb and renal vasomotor responses followed different patterns. The baroreceptor reflex sensitivity for renal vasoconstriction was greatest during rest and least during sleep. The reflex sensitivity in the hindlimb was unaltered by behavior. Thus behavior modifies baroreceptor reflex responses in the heart and peripheral circulation in different patterns.
Dehydration enhances endotoxin fever by increased production of endogenous pyrogen
Authors: Morimoto A. , Murakami N. , Ono T. , Watanabe T.
Published: December 2017

The febrile responses in rats to an intravenous injection of the bacterial endotoxin Salmonella typhosa were investigated under normally hydrated and dehydrated conditions. When endotoxin was injected intravenously into the dehydrated rats, a biphasic-patterned fever resulted, whereas in normal rats an intravenous injection of endotoxin did not induce fever. No significant differences in febrile responses to the intravenous endogenous pyrogen (EP), prostaglandin E2, and intracerebroventricular prostaglandin E2 between normal and dehydrated rats were observed. When the blood plasma obtained from rats with endotoxin-induced fever under dehydrated conditions was transferred to the normal rats, a significant rise in the body temperature was induced. The effect of hydration by an administration of the hypotonic solution after dehydration was examined in endotoxin-induced fever and in changes of the basic blood parameters. It is concluded that febrile responses to endotoxin during dehydrated condition are caused by an increased production of EP. The migration of leukocytes from circulation to any other tissue will be an important factor in producing EP under dehydrated conditions. Furthermore, under dehydrated condition, EP may be produced by numerous macrophages in tissues in vivo, where many kinds of leukocytes migrate and exchange signals with each other in developing an immune response.
Effect of glucose and other hexoses on efferent discharges of brown adipose tissue nerves
Authors: Niijima A.
Published: December 2017

The activity of sympathetic nerves innervating interscapular brown adipose tissue of the rat was recorded. Intravenous administrations of glucose (100-300 mg/kg) enhanced the nerve activity. However, mannose, fructose, or galactose (300 mg/kg) showed no effect, suggesting the response is related to diet-induced thermogenesis in the brown adipose tissue.
Pressor responses to central hypertonic NaCl stimulation in conscious turkeys
Authors: Lee J. C. , Denbow D. M. , Ashen M. D. , Roudabush A. D.
Published: December 2017

The purpose of this investigation was to examine the possible involvement of the central renin-angiotensin system in the pressor response to the intracerebroventricular (icv) injection of hypertonic NaCl in conscious turkeys. The icv injection was accomplished via a stereotaxically implanted stainless steel guide cannula in the lateral cerebral ventricle. The arterial blood pressure (AP) of the turkey was measured by means of a PE catheter in the left brachial artery. The icv administration of hypertonic NaCl caused a dose-dependent increase of AP. The mean AP increases due to 10-microliter icv injections of 0.9, 3.6, and 7.2% NaCl were 1.4 +/- 1.4, 18.1 +/- 3.0, and 31.2 +/- 3.2 (SE) mmHg, respectively. These changes were statistically significant (P less than 0.001). The icv administration of captopril, [Sar1, Ile8]angiotensin II, or pentobarbital sodium markedly reduced the pressor response to the icv injection of hypertonic 7.2% NaCl. Blockade of central adrenergic receptors with phentolamine and propranolol was without effect. These results support the contention that the central renin-angiotensin system may directly contribute to pressor responses induced by central hypertonic NaCl stimulation.
Effect of focal cooling of central chemosensitive areas on cerebral ischemic response
Authors: Prabhakar N. R. , Mitra J. , Van de Graaff W. , Haxhiu M. A. , Cherniack N. S.
Published: December 2017

The ventrolateral medullary surface (VMS) has been shown to have chemosensitive areas that can alter blood pressure and respiration. It has also been shown that lesions near the VMS can affect the intensity of the cerebral ischemic response (CIR). To determine which regions of the central chemosensitive areas of the ventral medullary surface contribute to the pressor response caused by cerebral ischemia, we used focal cooling of the caudal Loescheke's (CL), intermediate Schlaefke's (IS), and rostral Mitchell's (RM) areas of VMS during ischemia of the brain. Experiments were performed on 17 pentobarbital sodium-anesthetized, paralyzed, and artificially ventilated cats after denervation of the vagi and sinoaortic nerves. Bilateral occlusion of the external carotid and vertebral arteries resulted in a significant increase of arterial pressure (from 129 +/- 4 to 174 +/- 8 mmHg, P less than 0.01) and an increase in splanchnic sympathetic activity. However, heart rate and cervical sympathetic activities were not appreciably affected by cerebral ischemia. Bilateral cooling of the IS area to as low as 10 degrees C led to a decrease or disappearance of phrenic activity but failed to affect the magnitude of the pressor response. Also cooling of the CL and RM areas and application of Gelfoam pledgets soaked in lidocaine (4%) to these areas did not affect the CIR. However, covering the whole VMS with 0.2 ml of 4% lidocaine or cold cerebrospinal fluid (10 degrees C) abolished the ischemic reflex.(ABSTRACT TRUNCATED AT 250 WORDS)
Role of atrial natriuretic peptide in volume-expansion natriuresis
Authors: Schwab T. R. , Edwards B. S. , Heublein D. M. , Burnett J. C.
Published: December 2017

Studies were performed to investigate the role of circulating atrial natriuretic peptide (ANP) in acute volume-expansion natriuresis. Sham-operated (SHAM, n = 6) and right atrial appendectomized (ATRX, n = 12) anesthetized rats underwent acute volume expansion with isoncotic albumin. After equilibration and control periods, volume expansion increased urine flow rate, urinary sodium excretion, fractional excretion of sodium, and circulating ANP. Absolute increases in urine flow rate (delta 46 +/- 4 SHAM; delta 25 +/- 5 microliter/min ATRX), urinary sodium excretion (delta 9.48 +/- 1.01 SHAM; delta 4.77 +/- 1.03 mueq/min ATRX), fractional excretion of sodium (delta 3.16 +/- 0.53 SHAM; delta 1.65 +/- 0.32% ATRX), and ANP (delta 303.3 +/- 35.9 SHAM; delta 156.6 +/- 26.0 pg/ml ATRX) were significantly reduced by right atrial appendectomy. No significant differences in mean arterial pressure, central venous pressure, or glomerular filtration rate during volume expansion were observed between groups. These studies support the hypothesis that right atrial appendectomy in the rat attenuates acute volume expansion-induced increases in circulating ANP and urinary sodium excretion and that the natriuresis of acute volume expansion is mediated in part by an increase in circulating ANP.
Kinetic model of whole-body vanadium metabolism: studies in sheep
Authors: Patterson B. W. , Hansard S. L. , Ammerman C. B. , Henry P. R. , Zech L. A. , Fisher W. R.
Published: December 2017

A compartmental model for vanadium metabolism in sheep has been proposed. The model is consistent with data obtained from sheep fed a control diet (2.6 ppm vanadium) containing 0 or 200 ppm supplemental vanadium. Sheep were administered 48V dioxovanadium either orally or intravenously. Blood, feces, and urine radioactivity were monitored for 6 days postdosing. Several new insights regarding vanadium metabolism are suggested and tested against the data using the model. Some of these include significant absorption of 48V occurs from the upper gastrointestinal tract; an in vivo process is necessary in order for 48V dioxovanadium to be converted into a more biologically reactive species; at steady state the upper and lower gastrointestinal tracts contain at least 10- and 100-fold more mass of vanadium, respectively, than does blood. No statistically significant differences in transport rate constants were found between animals receiving 0 and 200 ppm supplemental dietary vanadium. The availability of a model will enable the refinement of future studies regarding vanadium metabolism in the ruminant.
Glucagon and epinephrine suppression of food intake in liver-denervated rats
Authors: Bellinger L. L. , Williams F. E.
Published: December 2017

Milk intake suppression after intraperitoneal glucagon and epinephrine injections was studied in liver-denervated [hepatic vagal branch transection (VAG-B), hepatic artery-portal vein denervations (H-ART), or total denervation (TOTAL)] and sham-operated rats (SHAM). In experiment 1, glucagon (500 micrograms/kg, Sigma) had no effect on 30 min of milk intake but produced hyperglycemia in all groups. Glucagon (750 micrograms/kg, Sigma; 400 micrograms/kg, Lilly) decreased intake in all groups, as did epinephrine (30 micrograms/kg). In experiment 2, TOTAL and SHAM were tested with 50, 100, and 400 micrograms/kg of glucagon (Lilly). Only the two larger doses suppressed milk intake of both groups, whereas all doses caused hyperglycemia. Epinephrine (30 micrograms/kg) decreased food intake more than glucagon but caused less hyperglycemia than any glucagon dose. In experiment 3, VAG-B and SHAM groups were given glucagon (400 micrograms/kg, Lilly), which reduced their intake. Under these test conditions, liver innervation is not required for glucagon and epinephrine to suppress milk intake. The ability of the two hormones to suppress ingestion appears to be dissociated from their hyperglycemic actions.
Fetal vascular pressure and heart rate responses to nonlabor uterine contractions
Authors: Brace R. A. , Brittingham D. S.
Published: December 2017

The purpose of this study was to determine whether there are changes in fetal arterial pressure, venous pressure, or heart rate during nonlabor uterine contractions (i.e., contractures) in late gestation pregnant sheep. To do this, amniotic fluid pressure was continuously recorded using on-line computer techniques and subtracted from fetal arterial and venous pressures. With randomly selected data, there were no statistically significant changes with time in the fetal variables. However, when averaged with respect to time of the contractures, fetal arterial and venous pressures increased significantly during the contractures, and heart rate decreased. In addition, there were small but statistically significant decreases in each of the three fetal variables just before the contractures. Blocking the fetal autonomic nervous system eliminated the decreases in the variables before the contractures as well as the decrease in heart rate during the contractures, but arterial and venous pressure increased normally. Infusion of 1 liter of warmed saline into the amniotic space did not alter the fetal cardiovascular or amniotic fluid pressure changes during contractures. In summary, there are significant fetal cardiovascular changes during nonlabor uterine contractions, and these are consistent with a translocation of fetal blood from the placenta into the fetal body. Although the cause of fetal cardiovascular changes just before the contractures is unknown, they suggest but do not prove that the fetus may provide the signal for the nonlabor uterine contractions to occur.
Recovery of blood volume and osmolality after thermal dehydration in rats
Authors: Nose H. , Morita M. , Yawata T. , Morimoto T.
Published: December 2017

Changes in blood volume and fluid intake were assessed continuously during recovery from thermal dehydration (approximately 6 ml/100 g body wt) in rats. Catheters chronically implanted into the jugular vein and descending aorta were connected with the system for continuous monitoring of blood volume. Changes in blood volume and fluid consumption were recorded for 2-6 h while tap water (TW group) or 0.45% NaCl solution (Na group) was provided ad libitum. As soon as the fluids became available, the rats in both groups drank a relatively large volume (2-3 ml/100 g) within 10 min. Thereafter, Na group consumed approximately 1 ml X 100 g body wt-1 X 30-60 min-1 and regained almost all water loss in 2 h, whereas TW group drank only approximately 50% of their water deficit. The percent of ingested fluid that remained in vascular space was 17% on average in both groups. Thus TW group replenished 80% of the depleted blood volume, whereas Na group regained almost all of it. Rehydration for 2 h decreased plasma Na concentration to the control level in TW group, whereas in Na group the level remained high. These results suggest that the lower fluid intake in TW group is due to the dilutional inhibition of drinking and that the osmoregulation has priority over blood volume regulation in restitution from thermal dehydration.
Spinal vasopressin mechanisms of cardiovascular regulation
Authors: Porter J. P. , Brody M. J.
Published: December 2017

Extrahypothalamic vasopressin-containing neurons have been implicated in the central neural control of the cardiovascular system. In the present study we investigated the possibility that vasopressinergic neurons arising from the paraventricular nucleus (PVN) and terminating in the spinal cord are involved in the regulation of vasomotor functions. Vasopressin (1-17 pmol) was injected into the spinal subarachnoid space of conscious rats instrumented with Doppler flow probes and indwelling intrathecal catheters. The peptide produced a dose-related increase in arterial pressure accompanied by vasoconstriction in the mesenteric, renal, and hindquarter vascular beds. Pretreatment, intrathecally, with 0.5 nmol of the vasopressin antagonist d(CH2)5Me(Tyr)AVP completely prevented the increase in arterial pressure expected after subsequent intrathecal injection of vasopressin. However, the changes in arterial pressure and vascular resistances produced by stimulation of the PVN were not affected by the intrathecal antagonist. Stimulation of the PVN in Brattleboro rats, which lack hypothalamic and spinal vasopressin, produced hemodynamic responses similar to those produced in Long-Evans control rats. Taken together, these data suggest that spinal vasopressin can act within the spinal cord to alter vasomotor functions; however, the hemodynamic effects evoked by stimulation of the PVN do not appear to depend on spinal vasopressinergic mechanisms.
Elevated CSF osmolality inhibits thermoregulatory heat loss responses
Authors: Turlejska E. , Baker M. A.
Published: December 2017

The effect of intracerebroventricular (icv) infusions of hypertonic NaCl or sucrose on thermoregulatory responses to heat was studied in conscious rabbits to test the idea that brain osmoreceptors are involved in the inhibition of evaporative heat loss and elevation of body temperature in dehydrated mammals at high ambient temperature (Ta). In rabbits hydrated ad lib and resting at a Ta of 33 degrees C, icv infusion (3.4 microliter/min) of hypertonic (1,500 mosm) NaCl or sucrose in artificial cerebrospinal fluid (ACSF) produced a significant reduction in respiratory frequency (f) and in ear skin temperature (Te) and a rise in brain temperature (preoptic area, Tpoa). icv infusion of ACSF alone or ACSF + NaCl at 500 and at 750 mosm had no effect on f or on Te or Tpoa. Infusion of NaCl + ACSF at 1,000 mosm reduced f but did not affect Te or Tpoa. In hydrated rabbits, icv infusion of 1,500 mosm NaCl abolished the rise in f and in Te elicited by POA heating at Ta of 25 degrees C. In dehydrated rabbits at 33 degrees C, f was below hydrated levels and icv infusion of water (6.8 microliter/min) produced a reversible elevation in f. These findings suggest that brain osmoreceptors can influence thermoregulation in hot environments.
Salt appetite is suppressed by interference with angiotensin II and aldosterone
Authors: Sakai R. R. , Nicolaidis S. , Epstein A. N.
Published: December 2017

Blockade of central but not peripheral mineralocorticoid receptors, with the antimineralocorticoid RU-28318, reduces but does not suppress salt appetite aroused by sodium depletion in the rat. When central mineralocorticoid blockade is combined with captopril treatment to prevent formation of endogenous angiotensin II the appetite is completely suppressed. Suppression of the appetite occurred without changes in the animals' spontaneous ingestive behaviors, sodium excretion, or insulin-induced food intake. These results demonstrate that a synergy of angiotensin II and aldosterone is responsible for the expression of depletion-induced salt appetite in the rat.
Atrial natriuretic factor and renal function during head-out water immersion in conscious dogs
Authors: Miki K. , Hajduczok G. , Klocke M. R. , Krasney J. A. , Hong S. K. , de Bold A. J.
Published: December 2017

The potential role of atrial natriuretic factor (ANF) in the renal response to head-out water immersion (WI) was studied. Five female mongrel dogs, trained to stand for 100 min in air followed by 100 min of thermoneutral WI at 37 degrees C or 200 min in air (timed control, TC), were chronically instrumented with arterial and venous catheters. The animals were hydrated with a volume of 0.45% NaCl solution equivalent to 2% of their body weight. Prehydration levels of arterial ANF were 243 +/- 15 (SE), and venous ANF levels were 211 +/- 21 pg/ml. WI resulted in an increase in urine flow from 0.7 +/- 0.1 ml/min to a peak flow of 2.2 +/- 0.3 ml/min (P less than 0.05). On immersion, plasma venous and arterial ANF levels increased significantly by 29 and 21% from the preimmersion values of 183 +/- 14 and 222 +/- 20 pg/ml, respectively. The arterial-venous difference for plasma ANF was maintained at 35 +/- 14 pg/ml (P less than 0.05) during WI; therefore venous sampling may suffice as a measure of circulating ANF levels. Sodium excretion increased linearly during WI to a peak value of 228 +/- 32 mu eq/min from a base line of 52 +/- 12 mu eq/min (P less than 0.05). These data indicate that peripheral tissues extract ANF and that WI is a physiological stimulus for the release of ANF. However, the time course and magnitude of the changes in plasma ANF and urine sodium excretion during WI are not comparable, and other mechanisms are likely responsible for the WI natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)
Fatty acid oxidation and glucose utilization interact to control food intake in rats
Authors: Friedman M. I. , Tordoff M. G.
Published: December 2017

To determine whether glucose and fat metabolism interact to control food intake, rats were administered 2-deoxyglucose (2-DG), which inhibits glucose utilization, and methyl palmoxirate (MP), which inhibits fatty acid oxidation. Combined treatment with 2-DG and MP increased food intake in a synergistic fashion. This synergistic effect was observed even at doses of the two agents that alone did not increase food intake, and it was expressed by either an initiation of eating or a prolonged bout of eating, depending on the testing conditions. Metabolic measures of circulating substrates, liver glycogen, and gastric contents confirmed that the drugs had their intended metabolic effects and revealed no evidence that one drug enhanced the direct metabolic action of the other. The results provide direct evidence that glucose and fat metabolism exert a coordinated control over feeding behavior and suggest the existence of a common integrative mechanism in that control.
Hemodynamics of hemorrhage in the conscious rat and chicken
Authors: Ploucha J. M. , Fink G. D.
Published: December 2017

Hemodynamic responses to hemorrhage in conscious chicks (n = 10, 233 g) and rats (n = 10, 309 g) were compared. The animals were fitted with miniature pulsed Doppler aortic flow probes 2 days (chickens) or 5 days (rats) before catheterization, and the experiment began 1 (chickens) or 2 (rats) days later. Mean arterial pressure (MAP) and cardiac output (CO) were recorded continuously and simultaneously digitized to compute total peripheral resistance (TPR). MAP, CO, and TPR values were graphed on-line by a microcomputer and stored for later analysis. A 4-ml hemorrhage reduced MAP and CO by 25 and 43% in the rat, and 15 and 4% in the chickens, respectively. The fall in CO in the rat was due to reduction of stroke volume (SV) unlike the birds where SV was well maintained. TPR was elevated 65% in the rats and fell 13% in the chickens. The minimal fall in CO and SV in these conscious birds suggests that anesthetic agents used previously (i.e., urethane, paraldehyde, phenobarbital, and pentobarbital sodium) suppressed cardiac function. However, they do not account for the lack of a peripheral vascular response during hemorrhage. The chicken apparently maintains MAP by a volume regulating mechanism operating independently of peripheral vascular tone inasmuch as circulating fluid volume restitution is rapid and occurs without vasoconstriction. The rat maintains MAP through reflex cardiac and peripheral vascular responses which eventually may contribute to transvascular fluid loss and the ultimate collapse after prolonged hemorrhagic hypotension.
Sodium absorption coupled to ammonia excretion in osmoconforming marine invertebrates
Authors: Hunter K. C. , Kirschner L. B.
Published: December 2017

Evidence was sought for the presence of amiloride-sensitive Na-NH4 and NaH exchange systems in four species of marine osmoconformers. When the crabs Cancer antennarius and Petrolisthes cinctipes were in seawater (SW), amiloride (10(-4) M) reduced NH3 efflux by approximately 33 and 60%. Inhibition was reversible on removing the amiloride. In dilute (60%) SW, inhibition of NH3 output by C. antennarius was even greater than in SW. Na+ uptake by P. cinctipes was reduced by approximately 20% in the presence of amiloride (the measurement was not made on C. antennarius). Amiloride had no effect on proton efflux in either crab. The data suggest that Na-NH4 exchange occurs in these animals but that Na-H exchange does not occur. The inhibitor had no effect on NH+4 excretion by the polychaete worm Nephtys caecoides and the mussel Mytilus californianus; it was also without effect on proton output by the worm. The data suggest that the exchange systems are absent from these animals. Implications of these observations for the evolution of such cation exchange systems are discussed.
Mode of adrenergic and peptidergic inhibition of ion transport in flounder gill
Authors: Davis M. S. , Shuttleworth T. J.
Published: December 2017

The mechanisms of inhibition of branchial ion transport by epinephrine and somatostatin were investigated in the isolated perfused gill preparation of seawater-adapted flounder Platichthys flesus. The electrogenic transepithelial potential recorded in gills perfused and bathed with identical salines was stimulated by glucagon, forskolin, or a cyclic adenosine 5' monophosphate (AMP) derivative, each administered at a concentration identified in preliminary experiments as being submaximally effective. The subsequent abilities of epinephrine and somatostatin to inhibit the stimulated potential were found to be dependent on the site of action of the stimulatory agent with respect to the formation of cyclic AMP. Thus the maximal adrenergic or peptidergic inhibition of the potential stimulated by exogenous cyclic AMP was significantly reduced compared with the maximal inhibition of the potential stimulated by either forskolin or glucagon. The data indicate dual modes of action by which epinephrine and somatostatin achieve maximal inhibition of branchial ion transport; a cyclic AMP-independent mechanism that is effective in the presence of cyclic AMP and an additional mechanism to inhibit cyclic AMP synthesis.
Analysis of hemodynamic variability after sinoaortic denervation in the conscious rat
Authors: Trapani A. J. , Barron K. W. , Brody M. J.
Published: December 2017

The present study was undertaken to determine the regional hemodynamic basis for increased mean arterial pressure (MAP) variability produced by sinoaortic baroreceptor denervation (SAD) in the conscious rat. Sinoaortic-denervated and intact rats were instrumented chronically with a catheter placed in the femoral artery and pulsed-Doppler flow probes positioned on the renal and superior mesenteric arteries and the lower abdominal aorta to determine MAP, heart rate, and regional vascular resistance. Each cardiovascular variable was sampled once per minute during a 1-h recording period. Compared with control animals, baroreceptor-denervated animals exhibited greater variability of MAP and mesenteric, renal, and hindquarter resistances 7–9 days after SAD. The variability of heart rate was similar when animals from the two groups were compared. The pattern of significant correlation for the relationship of MAP to vascular resistance in the different beds was not consistent for individual SAD and intact animals. Finally, a wider distribution of mean values was observed for the individuals within the SAD group for MAP, heart rate, and hindquarter and renal vascular resistances. We conclude that SAD produces greater fluctuation of vascular resistance in several beds which contributes to the increased lability of MAP; however, there is no predictable pattern of vascular resistance lability which underlies the variability of arterial pressure.
Vasopressin responses to corticotropin releasing factor and hyperosmolality in conscious dogs
Authors: Raff H. , Skelton M. M. , Merrill D. C. , Cowley A. W.
Published: December 2017

We recently reported that ovine corticotropin releasing factor (CRF) infusion in conscious dogs elevated plasma vasopressin. The present study examines the vasopressin, adrenocorticotropic hormone (ACTH), and cortisol responses to CRF infusion (20 ng X kg-1 X min-1), to hypertonic saline infusion (NaCl 0.054 meq X kg-1 X min-1), and to simultaneous coinfusion of CRF and NaCl (CRF + NaCl) without (no-dex) or with (dex-treated) dexamethasone pretreatment in six conscious dogs (6-8 experiments/dog). CRF had no significant effect on plasma sodium or osmolality, blood pressure, or heart rate. NaCl increased plasma sodium from 146 +/- 1 to 151 +/- 1 meq/l and plasma osmolality from 298 +/- 3 to 305 +/- 3 mosmol/kg. Vasopressin increased significantly during CRF (2.1 +/- 0.5 to 4.8 +/- 1.1 pg/ml) and NaCl (1.9 +/- 0.3 to 5.0 +/- 0.8 pg/ml). Coinfusion of CRF and NaCl resulted in a response larger than the sum of the two infusions alone (3.0 +/- 1.6 to 31.4 +/- 18.5 pg/ml). The ACTH response to CRF (45 +/- 8 to 288 +/- 88 pg/ml) was not augmented by coinfusion with NaCl. DEX attenuated the vasopressin and ACTH responses to each infusion. We conclude that CRF-induced increases in vasopressin are augmented by a simultaneous osmotic stimulus. In addition, the plasma vasopressin responses to CRF and/or hypertonic saline infusion are inhibited by glucocorticoid pretreatment.
Cardiovascular effect of V1 vasopressinergic blockade during acute hypercapnia in conscious rats
Authors: Walker B. R.
Published: December 2017

Experiments were performed to test the possible involvement of arginine vasopressin (AVP) in the systemic cardiovascular responses to acute hypercapnic acidosis in conscious chronically instrumented rats. Exposure to 6% CO2 caused arterial PCO2 to rise from 34 +/- 2 to 53 +/- 1 Torr. This level of hypercapnia was associated with a consistent bradycardia; however, cardiac output, blood pressure, and total peripheral resistance were not significantly affected. Administration of 10 micrograms/kg iv of the specific V1 vasopressinergic antagonist d(CH2)5Tyr(Me)AVP during 6% CO2 had no effect on any of the measured hemodynamic variables. Furthermore, d(CH2)5Tyr(Me)AVP also had no effect in normocapnic control animals. Exposure to a more severe level of hypercapnia (10% CO2, arterial PCO2 = 89 +/- 1 Torr) resulted in marked hemodynamic alterations. Profound bradycardia and decreased cardiac output in addition to increases in mean arterial blood pressure and total peripheral resistance were observed. V1 vasopressinergic antagonism during 10% CO2 had no effect on heart rate but greatly increased cardiac output. In addition, blood pressure fell and resistance was decreased below prehypercapnic levels. These data suggest that a number of the hemodynamic alterations associated with severe hypercapnic acidosis in the conscious rat may be mediated by the peripheral cardiovascular effects of enhanced AVP release.
Augmented pressor response to vasopressin in awake dogs after cardiac denervation
Authors: Wang B. C. , Ginter G. F. , Goetz K. L.
Published: December 2017

Hemodynamic responses to varying intravenous infusion rates of vasopressin were studied in two groups of dogs; one group was cardiac denervated and the other sham operated. Vasopressin given at 200, 1,000, and 5,000 fmol X kg-1 X min-1 produced increases in aortic pressure that were significantly greater in cardiac-denervated dogs than in sham-operated dogs. The augmented pressor response in cardiac-denervated dogs was associated with greater increases in total peripheral resistance in this group; decreases in cardiac output were similar in the two groups of dogs. Vasopressin decreased heart rate significantly in each group, but the magnitude of the decrease was significantly smaller in cardiac-denervated dogs. In contrast to these results, the intravenous infusion of phenylephrine or angiotensin II in other experiments on the same dogs produced comparable increases in aortic pressure in each group. These results are consistent with earlier evidence indicating that vasopressin elicits more effective reflex mechanisms to attenuate the increases in blood pressure caused by its direct vasoconstrictor action than do other vasoconstrictor agents, such as angiotensin II and phenylephrine. Since the infusion of vasopressin produced a greater increase in arterial blood pressure in cardiac-denervated dogs than it did in sham-operated control dogs, it appears that at least part of the unique action of vasopressin may be mediated by the potentiation of a peripheral vasodepressor reflex arising from cardiac receptors.
Nuclear morphometric analysis of osteoblast precursor cells in periodontal ligament, SL-3 rats
Authors: Roberts W. E. , Fielder P. J. , Rosenoer L. M. , Maese A. C. , Gonsalves M. R. , Morey E. R.
Published: December 2017

Five small (55 days old, 196 +/- 5 g) (mean +/- SE) and five large (83 days old, 382 +/- 4 g) Sprague-Dawley strain, specific pathogen-free rats were exposed to a 7-day spaceflight and 12-h postflight recovery period. As measured in 3-micron sections, periodontal ligament (PDL) fibroblastlike cells were classified according to nuclear size: A + A' (40-79), B (80-119), C (120-169), and D (greater than or equal to 170 microns 3). Since the histogenesis sequence is A----A'----C----D----osteoblast, the relative incidence of A + A' to C + D is an osteogenic index. No difference in A + A' or C + D cells in small rats may reflect partial recovery of preosteoblast formation (A----C) during the 12-h postflight period. Large flight rats demonstrated increased numbers of A + A', indicating an inhibition of preosteoblast formation (A----C). At least in the older group, a 7-day flight is adequate to reduce PDL osteogenic potential (inhibition in PDL osteoblast differentiation and/or specific attrition of C + D cells) that does not recover by 12-h postflight
Mechanosensitive afferents of femoral-saphenous vein
Authors: Davenport P. W. , Thompson F. J.
Published: December 2017

Urotensin II (U II) caused marked concentration-dependent contractions of helical strips from several major arteries of the rat. The thoracic aorta was most sensitive; the apparent concentration of U II producing half-maximal contraction was 6.8 X 10(-10) M. Papaverine, dibutyryl cyclic AMP, forskolin, and nitroprusside antagonized the contractile responses to U II at the apparent concentrations producing 50% inhibition (IC50) of 7.6 X 10(-6), 2.1 X 10(-4), 2.5 X 10(-6), and 1.5 X 10(-8) M, respectively. Verapamil, a calcium channel-blocking agent, partially inhibited the contractile response to U II at IC50 = 6.5 X 10(-6) M. Maximal relaxation, i.e., a complete inhibition, could not be obtained even at a concentration of 3 X 10(-5) M verapamil. Cyproheptadine reduced the U II-induced contraction at higher concentrations. Phentolamine (10(-5) M), propranolol (10(-5) M), atropine (10(-4) M), tetrodotoxin (10(-6) M), burimamide (10(-5) M), and indomethacin (10(-5) M) did not change the U II-induced contraction. At higher concentration, U II (10(-8) M) induced a small contraction of aortic strips in Ca2+-free Krebs Henseleit solution similar to that of norepinephrine, but the U II-induced contraction was not inhibited by phentolamine or propranolol. The action of U II did not require the presence of endothelial cells. It is concluded that U II acts on vascular smooth muscle and induces the contraction partly through intracellular Ca2+ mobilization but mainly by stimulating the influx of extracellular Ca2+ via potential dependent and potential independent calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
Effects of temperature on contractile properties of skinned muscle fibers from three toad species
Authors: Johnston I. A. , Gleeson T. T.
Published: December 2017

Single fast fibers were isolated from the iliofibularis muscles of three species of toad with different thermal minima for active locomotion: 8 degrees C, American toad, Bufo americanus; 15 degrees C, Rocky Mountain toad, Bufo woodhousei woodhousei; 22 degrees C, Cane toad, Bufo marinus. All experiments were carried out during the summer. Fibers were chemically skinned and maximum isometric tension and unloaded contraction velocity were determined at a series of temperatures between 0 and 35 degrees C. At 25-30 degrees C, isometric tension development has a low temperature dependence (R10 = 1.1-1.3) and is in the range of 210-260 kN X m-2 for each of the three toads. However, at 0-10 degrees C, absolute values of tension increase in the series (B. americanus greater than B. woodhousei greater than B. marinus; i.e., with increasing cold tolerance), while thermal sensitivity between 0 and 10 degrees C is inversely related to cold tolerance. For example, at 0 degree C, maximum isometric tension (Po) for the most northerly distributed species is three times higher than for the subtropical to tropical species (P less than 0.001). R10 for Po (0-10 degrees C) is 1.7 for B. marinus, 1.3 for B. w. woodhousei, and 1.0 for B. americanus. In contrast, unloaded shortening speeds were similar at any given temperature for the three species. It is concluded that adaptations in Bufo myosin for activity at low temperatures largely involves changes in force production.
Comparison of effects of ATP-MgCl2 and adenosine-MgCl2 on renal function following ischemia
Authors: Sumpio B. E. , Hull M. J. , Baue A. E. , Chaudry I. H.
Published: December 2017

ATP-MgCl2 X administration had been shown to accelerate the recovery of renal function following warm ischemia. However, since the major breakdown product of ATP is adenosine, the relative contribution of ATP vs. adenosine in improving renal function following ischemia remains to be determined. To study this, kidneys were subjected to 45 min of normothermic ischemia and then perfused at 100 mmHg with oxygenated Krebs-HCO3 buffer containing albumin, [3H]inulin, substrates, and either 0.3 mM ATP-MgCl2 or adenosine-MgCl2 for 110 min. Perfusate and timed urine samples were collected and analyzed for radioactivity and [Na+]. The functional parameters indicated that although adenosine-MgCl2 treatment provided a transient improvement, it failed to provide a sustained improvement in renal function or attain control values compared with ATP-MgCl2 treatment. Thus, the salutary effects of ATP-MgCl2 following warm ischemia in the kidney are not mediated by adenosine.