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PubMed1985

Forskolin mimics the hydrosmotic action of vasopressin in the urinary bladder of toads Bufo marinus.

Net water flow JW was measured across the urinary bladder of toads Bufo marinus and averaged over periods of 1 min by means of a volumetric, automatic technique. The diterpene forskolin, an activator of adenylate cyclase bypassing the hormonal receptor subunit, induced a rapid, reversible, dose-dependent increase in osmotic water permeability, Pf, very similar to that induced by vasopressin. At 1.1 microM, forskolin induced a half-maximal response. At 5 microM forskolin caused a near maximal response and Pf increased from 1.66 +/- 0.15 to 66.6 +/- 2.99 microns s-1. In bladders pre-exposed to 5 microM-forskolin, further significant increases in Pf were obtained by their subsequent exposure to vasopressin, cyclic AMP, theophylline or serosal hypertonicity. The similarity of the forskolin and vasopressin actions was further demonstrated by the finding that substances causing enhancement (quercetin) or inhibition (trifluoperazine, vanadate, silver, cobalt, manganese and Ca2+-free Ringer solution) of the vasopressin response, induced parallel changes in the forskolin response. Three agents, however, induced dissimilar effects on vasopressin and forskolin: high K+ potentiated vasopressin but inhibited forskolin; methohexital and diamide inhibited vasopressin but had no effect on forskolin. The forskolin-induced hydrosmotic response can be viewed as a new criterion for ascertaining the messenger role of cycle AMP in the the hydrosmotic effect of vasopressin.

Animals↗
PubMed1986

Sensitization of aortic and cardiac baroreceptors by arginine vasopressin in mammals.

Vasopressin facilitates the baroreflex control of the circulation. The peptide may act at several sites to augment the baroreflex. In this study we examined the effect of vasopressin on aortic baroreceptors in anaesthetized rabbits and on left ventricular mechanoreceptors in anaesthetized cats. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from aortic baroreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single aortic nerve fibre discharge to elevation in arterial pressure. The slope relating nerve activity to mean arterial pressure increased from 0.24 +/- 0.05 (mean +/- S.E. of mean) to 0.50 +/- 0.16 impulses/cardiac cycle. mmHg (P less than 0.05) in ten aortic medullated fibres and from 0.06 +/- 0.03 to 0.18 +/- 0.04 impulses/cardiac cycle. mmHg (P less than 0.05) in three non-medullated fibres. Vasopressin (16 mu./kg. min) did not change resting nerve discharge in single fibres from left ventricular mechanoreceptors. Vasopressin (16 mu./kg. min) significantly enhanced the response of single nerve fibre discharge from left ventricular mechanoreceptors in response to elevation of left ventricular end-diastolic pressure. The slope relating nerve activity to left ventricular end-diastolic pressure increased from 0.24 +/- 0.07 to 0.32 +/- 0.07 impulses/cardiac cycle. mmHg (P less than 0.05) in six medullated fibres and from 0.10 +/- 0.01 to 0.15 +/- 0.02 impulses/cardiac cycle. mmHg (P less than 0.05) in four non-medullated fibres. These data show that vasopressin sensitizes high and low pressure baroreceptors and suggest a mechanism by which vasopressin may facilitate the baroreflex control of the circulation.

Action Potentials↗
PubMed1988

Dose-response effects of pressor doses of arginine vasopressin on renal haemodynamics in the rat.

1. Dose-response effects of arginine vasopressin on renal haemodynamics were studied in conscious and in pentobarbitone-anaesthetized rats infused with 77 mM-NaCl at 5.2 and 2.6 ml h-1 respectively. 2. Vasopressin at 0.8 pmol h-1 (100 g body weight)-1 did not have a significant effect on arterial blood pressure in conscious or anaesthetized rats. Increasing the dose to 2.5 pmol h-1 (100 g body weight)-1 induced a pressor effect in conscious rats but not in anaesthetized rats. A pressor response was observed in the latter at a dose of 10 pmol h-1 (100 g body weight)-1. 3. Pressor doses of vasopressin of 100 pmol h-1 (100 g body weight)-1 and less did not significantly alter the clearance of p-aminohippurate (PAH) in either conscious or anaesthetized rats. A dose of 1000 pmol h-1 (100 g body weight)-1 significantly decreased PAH clearance in both conscious and anaesthetized animals. 4. Inulin clearance was unchanged by non-pressor doses of vasopressin in both conscious and anaesthetized rats. Moderately pressor doses decreased inulin clearance in conscious animals only. The highest dose administered (1000 pmol h-1 (100 g body weight)-1) decreased inulin clearance in both conscious and anaesthetized rats. 5. Pressor doses of vasopressin had a biphasic effect on the filtration fraction in conscious rats. The filtration fraction decreased with doses of vasopressin at the lower end of the pressor range but increased with the highest dose of 1000 pmol h-1 (100 g body weight)-1. In contrast the filtration fraction did not change significantly with moderate pressor doses in anaesthetized rats but was increased by doses of 100 and 1000 pmol h-1 (100 g body weight)-1. 6. It is concluded that pressor doses of vasopressin lower than 100 pmol h-1 (100 g body weight)-1 do not decrease renal plasma flow rate in conscious or pentobarbitone-anaesthetized rats. The results suggest that the inconsistent effects of vasopressin on renal blood flow reported in the literature are due, at least in part, to the wide range of doses used.

Anesthesia↗
PubMed1993

Intracellular calcium and vasopressin release of rat isolated neurohypophysial nerve endings.

1. Monitoring of [Ca2+]i and vasopressin secretion in isolated nerve endings from the rat neurohypophysis were studied to determine the relationship between the time course of vasopressin secretion and depolarization-induced changes in [Ca2+]i. 2. Membrane depolarization by increasing the extracellular [K+] led to concentration-dependent, parallel increases in the amount of vasopressin release and in peak increases in [Ca2+]i. Half-maximal activation of a change in [Ca2+]i was attained at 40 mM extracellular K+. 3. The Ca2+ chelator dimethyl-BAPTA (1,2-bis(O-aminophenoxy)ethane-N,N,N'N'-tetraacetic acid), loaded into the nerve endings, reduced K+ depolarization-evoked vasopressin release and efficiently antagonized K(+)-induced changes in [Ca2+]i. Moreover, dimethyl-BAPTA dramatically reduced basal [Ca2+]i without a reduction in basal secretion. 4. The duration of the vasopressin secretory response was similar regardless of applied 50 mM K+ depolarizations longer than 30 s. The t1/2 of the secretory response was 45 s. Application of repetitive K+ depolarization pulses repetitive secretory responses of similar amplitude and duration. 5. The K(+)-induced changes in [Ca2+]i remained elevated throughout the duration of the depolarizing stimulus decreasing less than 30% over 3 min. The sustained increase in [Ca2+]i resulted largely from continued enhanced Ca2+ influx, demonstrated by susceptibility to the dihydropyridine, L-type calcium channel blocker, nicardipine. 6. Vasopressin secretion could be reinitiated following its decline to a step K+ depolarization by a further step increase in K+ or by removal and readdition of extracellular [Ca2+]. Alterations in [Ca2+]i paralleled periods of secretory activity. 7. Analysis of secretory responsiveness and change in [Ca2+]i to K+ depolarization in medium of altered extracellular [Ca2+] indicates that [Ca2+]i of 20 microM is sufficient to trigger vasopressin release. K(+)-induced alterations in [Ca2+]i could be observed at [Ca2+]o as low as 5 microM. Although smaller in amplitude to that observed at 2.2 mM [Ca2+]o the duration of the K(+)-induced secretory response increased at lower [Ca2+]o. 8. Transient vasopressin secretory responses were observed to sustained levels of [Ca2+] in digitonin and streptolysin-O-permeabilized nerve endings. Secretion could be re-evoked, following its decline, by a step increase in [Ca2+] or by removal and readdition of [Ca2+]o.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Regulation of activity-dependent dendritic vasopressin release from rat supraoptic neurones.

Magnocellular neurones of the hypothalamus release vasopressin and oxytocin from their dendrites and soma. Using a combination of electrophysiology, microdialysis, in vitro explants, and radioimmunoassay we assessed the involvement of intracellular Ca(2+) stores in the regulation of dendritic vasopressin release. Thapsigargin and cyclopiazonic acid, which mobilize Ca(2+) from intracellular stores of the endoplasmic reticulum, evoked vasopressin release from dendrites and somata of magnocellular neurones in the supraoptic nucleus. Thapsigargin also produced a dramatic potentiation of dendritic vasopressin release evoked by osmotic or high potassium stimulation. This effect is long lasting, time dependent, and specific to thapsigargin as caffeine and ryanodine had no effect. Furthermore, antidromic activation of electrical activity in the cell bodies released vasopressin from dendrites only after thapsigargin pretreatment. Thus, exposure to Ca(2+) mobilizers such as thapsigargin or cyclopiazonic acid primes the releasable pool of vasopressin in the dendrites, so that release can subsequently be evoked by electrical and depolarization-dependent activation. Vasopressin itself is effective in inducing dendritic vasopressin release, but it is ineffective in producing priming.

Animals↗
PubMed1988

Simultaneous and independent release of vasopressin and oxytocin in the rat.

The relative dependence or independence of the secretion of the neurohypophysial hormones, arginine vasopressin and oxytocin, was investigated using a wide variety of stimuli reported to cause the secretion of one or the other hormone. Differences in species, animal preparations, sampling techniques, assays, and other factors make comparison of many previous studies difficult. The aim of this study was to overcome these problems by using the same methodology, animal species, and assays to compare vasopressin and oxytocin release. To further strengthen the analysis, determinations of vasopressin and oxytocin were done in the same blood samples. The results demonstrated that during simultaneous release of both hormones, vasopressin is released in greater proportion following restraint stress, hemorrhage, isotonic hypovolemia, and nicotine, whereas oxytocin is released in greater proportion following endotoxin or hypertonic saline. Vasopressin was released without oxytocin following diethylstilbestrol. Oxytocin was released without concomitant vasopressin release following exercise, hypothermia, hyperthermia, labour, and lactation. Neither oxytocin nor vasopressin release was observed following thyroid-releasing hormone or insulin-induced hypoglycemia. These data illustrate the marked flexibility of the hypothalamo-neurohypophysial system that regulates secretion of vasopressin and oxytocin.

Animals↗
PubMed1992

Role of sodium and water excretion in the antihypertensive effect of vasopressin in the spontaneously hypertensive rat.

Mean arterial pressure (mmHg (1 mmHg = 133.322 Pa)), sodium excretion rate (mumol.kg-1.min-1), and urine flow (microL.kg-1.min-1) were measured in conscious unrestrained spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY) before, during, and after a 3-h intravenous infusion of arginine vasopressin (20 ng.kg-1.min-1), an equipressor dose of phenylephrine, or an infusion of the vehicle. Cessation of the phenylephrine infusion was associated with a return of arterial pressure to preinfusion control values in both SHR and WKY. Cessation of the vasopressin infusion was also associated with a return of arterial pressure to preinfusion values in WKY. In contrast, in the SHR, arterial pressure fell from a preinfusion control level of 164 +/- 6.2 to 137 +/- 4 mmHg within 1 h of stopping the vasopressin infusion. Five hours after stopping the infusion, pressure was 134 +/- 3 mmHg (29 +/- 5 mmHg below preinfusion levels). Similar to the WKY, cessation of a vasopressin infusion was associated with a return of arterial pressure to preinfusion values in Sprague-Dawley rats. Thus, the failure to observe a hypotensive response in normotensive rats was not a peculiarity of the WKY strain. Sodium excretion rates increased during the infusions of vasopressin to a greater extent in SHR than in WKY. However, the natriuresis induced by phenylephrine was not significantly different from that generated by vasopressin in SHR, and in WKY, the natriuresis was greater for phenylephrine than for vasopressin. Urine output increased to a greater extent during the infusions of phenylephrine in both SHR and WKY than during vasopressin infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1983

Vasopressin stimulates growth of renal epithelial cells in culture.

The hypothesis that arginine vasopressin could regulate kidney epithelial growth by its effect on Na+ transport was examined in cultures of cells from the BSC-1 line. Addition of vasopressin (75 pg/ml) or NaCl (25 mM) to the medium stimulated growth of confluent cultures but retarded growth of sparse cells in the presence of 0.5% calf serum. Thus the capacity of vasopressin or exogenous NaCl to regulate growth of BSC-1 cells was cell density dependent. Vasopressin stimulated growth of confluent cultures only in the narrow concentration range of 50-100 pg/ml (approximately 10(-10)M), whereas concentrations of 10 pg/ml and 125-1,000 pg/ml had no effect. In contrast, vasopressin at or above concentrations of 10 pg/ml raised cell Na+ content to its maximal value, which indicated that the hormone could increase the Na+ content of cells without necessarily stimulating their growth. To determine if vasopressin modulates growth by acting on the plasma membrane, nutrient transport and ligand binding were assessed in high-density quiescent cultures. The hormone augmented uptake of alpha-aminoisobutyric acid and binding of epidermal growth factor, whereas the addition of NaCl (25 mM) did not. Thus growth stimulation by vasopressin was associated with increased cell Na+ content, enhanced uptake of an amino acid, and augmented binding of a growth factor. These observations suggest that the growth-promoting effect of vasopressin is not a simple function of its capacity to alter cell Na+ flux but could be mediated by other actions of the hormone, perhaps at the level of the plasma membrane.

Animals↗
PubMed1987

Effect of insulin on osmoregulation of vasopressin.

Patients with uncontrolled insulin-dependent diabetes mellitus have elevations in plasma vasopressin that cannot be completely accounted for by recognized stimuli. To determine whether insulin deficiency per se increases plasma vasopressin, we investigated the effect of acute insulin depletion on the osmoregulation of plasma vasopressin in insulin-dependent diabetics. When intravenous insulin infusion was stopped, plasma vasopressin, osmolality, and glucose increased over the ensuing 5 h, whereas plasma sodium decreased, and blood volume and pressure did not change. This increase in vasopressin was not due to a loss of osmoregulation, because changes in plasma osmolality and sodium, induced by infusion of hypertonic saline or water loading, induced appropriate vasopressin responses under insulin deplete as well as replete conditions. However, when plasma osmolality and glucose were raised by infusion of hypertonic dextrose, plasma vasopressin increased significantly in diabetic patients under insulin-deplete but not under insulin-replete conditions and actually decreased in healthy controls. These results indicate that acute insulin depletion increases vasopressin secretion by sensitizing the osmoreceptor to stimulation by hyperglycemia. This change in osmoreceptor specificity may be explained by postulating that glucose transport by osmoreceptor neurons as insulin dependent.

Adult↗
PubMed1984

Differential effect of vasopressin on angiotensin and norepinephrine pressor action in rats.

The effect of vasopressin infusion on the pressor dose responses to angiotensin II and norepinephrine was studied in pentobarbital-anesthetized and unanesthetized nephrectomized rats. Pressor vasopressin (2-15 ng X kg-1 X min-1) given to anesthetized rats decreased sensitivity to angiotensin II in a dose-dependent manner (r = 0.88), an effect completely reversible by dPMeTyrAVP, a vasopressin vascular antagonist. Subpressor vasopressin (0.5-1 ng X kg-1 X min-1) given to unanesthetized rats diminished sensitivity to angiotensin II in the presence or absence of pentolinium (10 mg/kg). Shifts in dose-response curves to angiotensin II were always parallel. In contrast, dose responses to norepinephrine were not modified by vasopressin in pentolinium-treated rats and showed a small nonparallel rightward shift in animals without pentolinium. In animals without pentolinium, the baroreflex-mediated reduction in heart rate elicited by angiotensin II was not altered by vasopressin infusion. Our data suggest that vasopressin reduces angiotensin II pressor action by diminishing pressor sensitivity to the peptide. They indicate that the effect may be specific, mediated through the vascular receptor for vasopressin and independent of actions of this hormone on the autonomic nervous system.

Angiotensin II↗
PubMed1987

Vasopressin facilitates inhibition of renal nerve activity mediated through vagal afferents.

We measured the effect of vasopressin (8 mU X kg-1 X min-1) on reflex inhibition of renal sympathetic nerve activity induced by volume expansion in 13 sinoaortic-denervated anesthetized rabbits. Volume expansion increased left ventricular end-diastolic pressure (LVEDP) from 5.1 +/- 0.7 to 14.1 +/- 1.4 mmHg and decreased renal nerve activity (RNA) from 57.4 +/- 6.9 to 30.2 +/- 5.6 impulses/s. Infusion of vasopressin elevated LVEDP from 6.0 +/- 1.0 to 7.3 +/- 1.1 mmHg and decreased RNA from 61.8 +/- 7.2 to 47.1 +/- 6.3 impulses/s. Heart rate fell from 243 +/- 7 to 231 +/- 9 beats/min; no other significant hemodynamic changes were seen. During the infusion of vasopressin, volume expansion increased LVEDP to 13.7 +/- 1.2 mmHg and decreased RNA to 17.0 +/- 4.2 impulses/s. The slopes relating the percent decrease in RNA to the rise in LVEDP were calculated from values of RNA recorded at several levels of LVEDP. The slope averaged -6.2 +/- 1.1%/mmHg before vasopressin and nearly doubled (-11.9 +/- 1.8%/mmHg) during vasopressin. Infusion of placebo (saline) instead of vasopressin did not alter the reflex inhibition of nerve activity. Bilateral vagotomy abolished the decrease in resting nerve activity that occurred during infusion of vasopressin as well as the reflex inhibition of RNA. These data demonstrate that vasopressin facilitates the reflex inhibition of renal sympathetic nerve activity associated with increases in LVEDP and mediated through vagal afferents.

Animals↗
PubMed1989

Effects of vasopressin on pulmonary and systemic vascular mechanics.

The direct effects of vasopressin on the resistance and capacitance properties of the pulmonary and systemic vasculature were studied in nine aneural dogs on systemic and pulmonary bypass. The systemic and pulmonary pressure-flow, the systemic and pulmonary arterial pressure-volume, and the systemic and pulmonary venous pressure-volume relationships were determined for five levels of infused vasopressin. Vasopressin levels of approximately 10, 30, 150, 300, and 500 pg/ml were achieved by intravenous infusions. Samples of venous blood were drawn before and after each set of pressure-flow and pressure-volume relationships for the determination of vasopressin level by radioimmunoassay. A linear relationship was found between vasopressin level and systemic vascular resistance. Systemic vascular resistance increased 0.072 +/- 0.011 mmHg.kg.min.ml-1 for a change in vasopressin level of 100 pg/ml. Vasopressin did not affect pulmonary vascular resistance or any vascular compliance. High doses of infused arginine vasopressin were necessary to elicit substantial vasoconstriction.

Animals↗
PubMed1996

Influence of brain injury on vasopressin-induced pial artery vasodilation: role of superoxide anion.

The present study was designed to investigate the effect of fluid percussion brain injury (FPI) on vasopressin-induced pial artery vasodilation and the role of superoxide anion generation in those observed effects. In the piglet, it was observed previously the FPI produces pial artery constriction associated with free radical generation. Anesthetized piglets equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. FPI of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Vasopressin in physiological and pharmacological concentrations (10 and 1,000 microU/ml) produced vasodilation that was reversed to constriction after FPI (15 +/- 1 vs. -8 +/- 1 and 25 +/- 1 vs. 13 +/- 1% for 10 and 1,000 microU/ml before and after injury, respectively). Vasopressin-induced dilation was associated with increased cerebrospinal fluid guanosine 3', 5'-cyclic monophosphate, and these biochemical changes were blunted by FPI (407 +/- 12 and 720 +/- 28 vs. 4 and 272 +/- 5 fmol/ml for control and 10 microU/ml before and after injury, respectively). In contrast, polyethylene glycol superoxide dismutase (PEG-SOD) and catalase pretreatment 30 min before FPI partially restored vasopressin-induced pial artery dilation (14 +/- 1 vs. 3 +/- 1 and 22 +/- 1 vs. 2 +/- 4% for 10 and 1,000 microU/ml before and after FPI, respectively). Similarly, biochemical changes associated with vasopressin dilation were also partially restored by PEG-SOD and catalase after FPI. These data show that vasopressin is reversed from a dilator to a vasoconstrictor after FPI and suggests the superoxide anion generation contributes to the alteration of vasopressin cerebrovascular effects after injury and that such altered vasopressin cerebrovascular effects contribute to pial vasoconstriction after FPI.

Animals↗
PubMed1987

Glucocorticoid inhibition of neurohypophysial vasopressin secretion.

Several lines of evidence have suggested that neurohypophysial vasopressin secretion is under the influence of glucocorticoid negative feedback. Studies in clinical and experimental adrenal insufficiency have suggested that the impaired water excretion accompanying that syndrome may be due to elevated vasopressin levels. Furthermore, both the impaired water excretion and elevated vasopressin levels observed in adrenal insufficiency may be normalized by glucocorticoid treatment. This topic remains controversial, with a considerable body of evidence suggesting that vasopressin is elevated during adrenal insufficiency not because of a loss of central steroid negative feedback but because of alterations in plasma volume osmolality (renal mechanisms). Vasopressin responses to a variety of stimuli (hemorrhage, hypoxia, hypertonic saline) in normal humans and animals appear to be attenuated or eliminated by pretreatment with glucocorticoids. However, the vasopressinergic system appears to be considerably less sensitive to negative feedback than the corticotropin-releasing factor-adrenocorticotropic hormone (ACTH) system. There is evidence that the locus for this inhibitory effect is both directly at the posterior pituitary and within the hypothalamus. It is unlikely that corticosteroid negative feedback closes a direct hypothalamo-neurohypophysial-adrenocortical feedback loop. Since neurohypophysial vasopressin is involved in the control of ACTH secretion, it is more likely that the modulation of neurohypophysial vasopressin by glucocorticoid is an integral part of the overall negative-feedback control of ACTH secretion. The physiological role of glucocorticoid inhibition of vasopressin secretion remains speculative.

Adrenocorticotropic Hormone↗
PubMed1988

Intravenous vasopressin infusion decreases plasma ACTH concentration in conscious dogs.

Vasopressin infusion increases arterial and atrial pressures, which could stimulate arterial and cardiac baroreceptors to inhibit adrenocorticotropin (ACTH) secretion. Therefore, the current experiments were performed to test the hypothesis that vasopressin infusion decreases plasma ACTH concentration in conscious dogs. Vasopressin was infused for 90 min in three doses (0.5, 1.0, and 2.0 ng.kg-1.min-1) that produced increases in plasma levels within the physiological range. Only the highest dose of vasopressin increased mean arterial pressure, but left atrial pressure increased with all doses, and right atrial pressure increased with the two highest doses. A bradycardia was produced with all doses of vasopressin. Plasma ACTH concentration decreased from 44 +/- 12 to 25 +/- 7 (P less than 0.01), from 50 +/- 11 to 26 +/- 9 (P less than 0.001), and from 70 +/- 15 to 28 +/- 4 pg/ml (P less than 0.001) with infusion of 0.5, 1.0, and 2.0 ng.kg-1.min-1 vasopressin, respectively. In contrast, plasma cortisol concentration first increased (P less than 0.05) with each vasopressin dose, but after 15-30 min it decreased back to control levels. These results demonstrate that intravenous infusion of vasopressin decreases plasma ACTH concentration. Because the inhibition is associated with increases in atrial pressure and decreases in heart rate, it may be mediated via activation of the baroreceptor reflex.

Adrenocorticotropic Hormone↗
PubMed1989

Vasopressin reduces oxygen uptake in intact dogs but not in sinoaortic-denervated dogs.

We have investigated the effect of infusions of arginine vasopressin on cardiac output and O2 uptake in the presence and in the absence of sinoaortic reflexes to better understand the mechanism of the exaggerated decrease in cardiac output elicited by vasopressin. Chronically instrumented dogs received, on separate days, 30-min infusions of vasopressin (0.2, 1, 5, 20, and 60 ng.kg-1.min-1), phenylephrine (1, 3, and 10 micrograms.kg-1.min-1), and angiotensin II (ANG II) (10, 20, and 50 ng.kg-1.min-1). These infusions all increased mean arterial pressure to a maximum of 63 +/- 8.2 mmHg during the highest phenylephrine infusion rate. Vasopressin reduced cardiac output (electromagnetic flowmeter) more than the other vasoconstrictors for equivalent increases in arterial pressure. Vasopressin also produced dose-dependent decreases in O2 uptake, measured by collection of expired air. Such decreases were not observed with the other two agents. On the contrary, ANG II and phenylephrine increased O2 uptake significantly when they decreased cardiac output the most. The decrease in O2 uptake induced by vasopressin was significantly correlated with the decrease in cardiac output. Pretreatment of the dogs with atropine prevented the decrease in O2 uptake and blunted the fall in cardiac output induced by vasopressin at a rate of 5 ng.kg-1.min-1. In dogs surgically deprived of sinoaortic receptors, vasopressin given at 1 and 5 ng.kg-1.min-1 failed to reduce O2 uptake and cardiac output significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1992

Medullary pathways for adrenocorticotropic hormone and vasopressin secretion in rabbits.

We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.

2-Amino-5-phosphonovalerate↗
PubMed1994

Effects of gonadectomy on sexually dimorphic antidiuretic action of vasopressin in conscious rats.

The present study examined whether the antidiuretic response to vasopressin is affected by the estrous cycle and by gonadectomy in conscious, chronically instrumented hydrated rats. Infusion of vasopressin (10-100 pg.min-1.kg body wt-1) resulted in a dose-dependent antidiuresis. Urine volume and free water clearance decreased and urinary osmolality increased with no significant changes in mean arterial blood pressure, heart rate, osmolar clearance, and urinary sodium and potassium excretion. The antidiuretic response to vasopressin was significantly greater in intact male and estrous female rats than in intact female rats in the other phases of the estrous cycle. Thus the calculated doses of vasopressin to reduce urine flow and free water clearance, as well as to increase urinary osmolality 50% from their control values, were significantly higher in nonestrous females than in males and estrous females. Gonadectomy was without effect on the antidiuretic potency of vasopressin in males, but in gonadectomized females the antidiuretic response to vasopressin was enhanced to a level similar to that observed in intact males. These data indicate that the antidiuretic activity of vasopressin is affected not only by gender but also by phase of the estrous cycle and that the ovarian hormone(s) may modulate the antidiuretic action of vasopressin.

Animals↗