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PubMed1979

Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP.

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.

Animals↗

PubMed1980

Effect of vasopressin on renal kallikrein excretion.

In an attempt to investigate a possible interaction between vasopressin and the renal kallikrein-kinin system, renal function and urinary kallikrein excretion were monitored in trained conscious dogs and in anesthetized rats in water diuresis and in vasopressin-induced antidiuresis. Vasopressin elevated urinary kallikrein excretion in a dose-dependent way in both species, with concomitant increases in urinary osmolality and electrolyte excretion. A significant increase in kallikrein excretion was observed with a dose of vasopressin as low as 2 mU . kg-1 . h-1 in the dog and 3 mU . kg-1 . h-1 in the rat without a change in renal hemodynamics. In the rat vasopressin-induced changes in kallikrein excretion were positively correlated with changes in sodium and potassium excretion and negatively correlated with changes in free water clearance. It is concluded that vasopressin over its normal physiological range of concentration stimulates renal kallikrein secretion.

Animals↗

PubMed1980

Vasopressin and collecting duct intramembranous particle clusters: a dose-response relationship.

Vasopressin increases the permeability of collecting ducts to water. Administration of this hormone is also associated with an increase in intramembranous particle clusters in rat collecting duct luminal membrane (CDLM) as revealed by freeze-fracture electron microscopy. To determine whether this morphologic alteration of CDLM is quantitatively related to the dose of vasopressin, anesthetized Brattleboro homozygous rats were given the hormone at different doses. CDLM from kidneys removed before and during infusion were examined by freeze-fracture electron microscopy. The frequency of CDLM clusters as well as the area of membrane occupied by them was related to the dose of vasopressin. In a separate experimental protocol, a decrease in intramembranous particle clusters accompanied a decrease in urinary osmolality when vasopressin was stopped. We conclude that CDLM intramembranous particle clusters represent a specific structural change related to the action of vasopressin. Accordingly, quantitation of CDLM clusters may serve as an end point for the study of vasopressin-induced water permeability.

Animals↗

PubMed1982

Effect of aging on urinary concentrating mechanism and vasopressin-dependent cAMP in rats.

The effect of aging on urinary concentrating ability and the pathogenic mechanism involved were investigated in Fischer 344 rats. While the rats had free access to drinking water, 24-mo-old rats were polydipsic and polyuric compared with 6- and 12-mo-old rats. The maximum urinary concentrating ability after 40-58 h of water deprivation was not different between 6- and 12-mo-old rats (Uosmol 2,941 +/- 173 vs. 2,706 +/- 96 (SE) mosmol/kg), but it was significantly decreased in 24-mo-old rats (1,885 +/- 172 mosmol/kg, P less than 0.01). Similarly, although 5 mU/ml vasopressin increased the concentration of cAMP and papillary slices in 12-mo-old rats (delta +2.81 +/- 0.62 pmol/mg tissue, P less than 0.01), the same concentration of vasopressin failed to increase the cAMP concentration in 24-mo-old rats (delta +0.25 +/- 0.21 pmol/mg tissue, P greater than 0.05). In the adenylate cyclase preparation of renal papilla, the response to low concentrations of vasopressin was diminished in 24-mo-old rats. The dose-response curve was shifted to the right and the ED50 concentration of vasopressin was increased in 24-mo-old rats compared with 12-mo-old rats: 1.40 +/- 0.12 mU/ml vasopressin vs. 3.04 +/- 0.22. These results suggest that the decrease in vasopressin-dependent cAMP generation may in part be responsible for the impairment of urinary concentrating ability in 24-mo-old rats.

Adenylyl Cyclases↗

PubMed1984

Vasopressin and urine flow rate responses to stress in conscious dogs.

Behavioral stress increases arterial pressure while decreasing urine flow rate; the urine flow rate response can be abolished by surgical renal denervation. In this study, the effects of infusion of alpha-adrenoceptor antagonists (intravenous phenoxybenzamine or prazosin) on the antidiuretic and plasma vasopressin responses to stress were examined. Without alpha-adrenoceptor blockade, 20 min of stress increased arterial pressure and decreased urine flow rate, but no change in urine osmolality or plasma vasopressin concentration occurred. Arterial pressure and urine flow rate returned to base-line level during a 20-min recovery period. With alpha-adrenoceptor blockade, which prevented the arterial pressure response to stress, urine flow rate still decreased during stress, but urine osmolality and plasma vasopressin concentration increased. The decrease in urine flow rate and increase in urine osmolality and plasma vasopressin concentration persisted into the first 20-min recovery period but returned to base-line level during a second 20-min recovery period. We conclude that the antidiuretic response to behavioral stress in conscious dogs with saline infusion alone is not mediated via a change in vasopressin release. In contrast, the antidiuretic response to behavioral stress with alpha-adrenoceptor antagonist infusion may be mediated via an increased release of vasopressin.

Animals↗

PubMed1985

Alpha 2-adrenoceptor antagonism of vasopressin-induced changes in sodium excretion.

Alpha 2-adrenoceptor agonists attenuate vasopressin-mediated changes in water excretion. The effects on sodium excretion, however, are unclear. We therefore utilized the nonrecirculating isolated perfused rat kidney to study the direct effects of vasopressin and alpha 2-adrenoceptor stimulation on sodium and water excretion in the absence of systemic regulatory systems. The perfusate was a Krebs-Henseleit solution (3.5 g/100 ml Ficoll; 1.0% albumin; 36 degrees C) containing prazosin (30 nM) and propranolol (100 nM) to prevent effects of alpha 1- and beta-adrenoceptor stimulation. Vasopressin (10 microU/ml) produced a significant (P less than 0.05) decrease in both water and sodium excretion. Potassium excretion was not significantly altered. Alpha 2-Adrenoceptor stimulation with l-epinephrine (28 nM) reversed (P less than 0.05) the effects of vasopressin on water and sodium excretion. To confirm that this attenuation was mediated by alpha 2-adrenoceptors, an alpha 2-adrenoceptor antagonist, yohimbine, was administered. Yohimbine (300 nM) blocked the effects of epinephrine on sodium and water excretion (P less than 0.05). The adenosine P-site agonist, SQ 22,536 (100 microM), which mediates its effects through inhibition of adenylate cyclase, produced the same reversal as that of epinephrine on vasopressin-mediated changes. Thus alpha 2-adrenoceptor stimulation antagonized the effects of vasopressin on both water and sodium excretion at the renal level. A corollary to this conclusion is that the function-specific activation of renal adenylate cyclase determines the effect of alpha 2-adrenoceptor stimulation.

Adenine↗

PubMed1985

Blockade of colchicine-induced inhibition of vasopressin-stimulated osmotic water flow: failure to influence microtubule formation.

Colchicine inhibits vasopressin-induced osmotic water flow across isolated toad urinary bladder. Concomitantly, colchicine has been shown to reduce the relative cytoplasmic volume fraction of microtubules in the apical granular cells of this epithelium that have been shown previously to mediate the hydroosmotic effect of vasopressin. Therefore, an intact cytoskeleton has been postulated to be a requirement for a full response to vasopressin. Since it has been demonstrated recently that cyclooxygenase inhibitors (meclofenamic acid) abrogate the inhibition by colchicine of vasopressin-stimulated water flow, we tested by stereological criteria the hypothesis that colchicine in the presence of meclofenamic acid does not prevent the polymerization of tubulin. Our results show that the relative cytoplasmic volume fraction of microtubules was reduced 75% by colchicine in the presence or absence of meclofenamic acid. An alternative explanation of the inhibitory action of colchicine is its ability in the toad urinary bladder to enhance the endogenous synthesis of and sensitivity to prostaglandin E, a potent negative modulator of vasopressin-stimulated water flow. An intact microtubular component of the cytoskeleton does not appear to be required for a maximal response to a physiological dose of vasopressin.

Animals↗

PubMed1988

Tonic inhibition of renal response to vasopressin by a pertussis toxin substrate.

The putative role of the inhibitory guanine nucleotide binding protein (Gi) in modulating the renal response to vasopressin was investigated using islet activating protein (IAP). IAP treatment in rats in vivo abolished the capacity of alpha 2-adrenoceptors to reverse vasopressin-induced adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in microdissected cortical collecting tubule (CCT) segments. IAP pretreatment also caused a marked upward shift in the dose-response curve of vasopressin (10(-10) to 10(-4) M)-induced cAMP accumulation. Augmentation of the response to vasopressin in rat CCT was dependent on the in vivo dose of IAP and paralleled the loss in alpha 2-adrenoceptor responsiveness. In the isolated perfused kidney the antinatriuretic and antidiuretic effects of the V2-receptor agonist desamino-8-D-arginine vasopressin (DDAVP) (1 pM) were enhanced following IAP pretreatment. alpha 2-Adrenoceptor stimulation (30 nM epinephrine) inhibited the renal effects of DDAVP (1 pM) in kidneys from control but not IAP-pretreated rats. Interestingly, IAP pretreatment alone caused increased urine flow rate and enhanced excretion of sodium and chloride without affecting potassium excretion or renal hemodynamics in vitro. Our results suggest that an IAP substrate, probably Gi, 1) is required for signal transduction by renal alpha 2-adrenoceptors, 2) may tonically modulate the response to vasopressin in the CCT but not of parathyroid hormone in the proximal convoluted tubule, and 3) participates in renal water and electrolyte reabsorption independent of exogenous adenylate cyclase stimulation.

Adenylate Cyclase Toxin↗

PubMed1999

Vasopressin stimulates sodium transport in A6 cells via a phosphatidylinositide 3-kinase-dependent pathway.

The enzyme phosphatidylinositide 3-kinase (PI3K) phosphorylates the D-3 position of the inositol ring of inositol phospholipids and produces 3-phosphorylated inositides. These novel second messengers are thought to mediate diverse cellular signaling functions. The fungal metabolite wortmannin covalently binds to PI3K and selectively inhibits its activity. The role of PI3K in basal and hormone-stimulated transepithelial sodium transport was examined using this specific inhibitor. Wortmannin, 50 nM, did not affect basal, aldosterone-stimulated, or insulin-stimulated transport in A6 cells. Wortmannin completely inhibits vasopressin stimulation of transport in these cells. Vasopressin stimulates PI3K activity in A6 cells. Vasopressin stimulation of transport is also blocked by 5 microM LY-294002, a second inhibitor of PI3K. One-hour preincubation with wortmannin blocked vasopressin stimulation of protein kinase A activity in the cells. Sodium transport responses to exogenous cAMP and forskolin, which directly activates adenylate cyclase, were not affected by wortmannin. These results indicate that wortmannin inhibits vasopressin stimulation of Na(+) transport at a site proximal to activation of adenylate cyclase. The results suggest that PI3K may be involved in receptor activation by vasopressin.

Androstadienes↗

PubMed1980

An inability of subcutaneous vasopressin to affect passive avoidance behavior.

The effects of subcutaneous injections of vasopressin on the passive avoidance behavior of rats were investigated in an extensive study. 200 male Wistar rats were tested in a step-through passive avoidance task. The animals were assigned randomly to 1 of 20 experimental groups consisting of five vasopressin injection and four shock level conditions. Each animal was trained to enter a dark compartment, then subjected to 0.25, 0.10, 0.05 mA or no foot shock for 2 sec. 60 min prior to a retention test administered 24 h after the foot shock, each animal was given a single injection of 0.30, 0.12, 0.06, or 0.03 IU of vasopressin or of saline. Time to reenter the shock compartment was tested 24 and 48 h after the foot shock. Latencies in both retention tests indicated that, although there was a significant effect of shock level on latency scores, there was no effect of vasopressin with any dose level tested. The inability to find an effect of vasopressin in this study is contrary to results of other studies. Several factors, including general reactivity of the animals or the distribution system for vasopressin in the brain, might provide the underlying reason for these dramatic differences.

Animals↗

PubMed1986

Central adrenergic control of vasopressin release.

The role of central adrenergic receptors in the control of vasopressin release was studied in the conscious rat. Norepinephrine (10 micrograms) and the alpha-1 agonist, phenylephrine (50 micrograms), administered intracerebroventricularly resulted in significant increases in the plasma vasopressin concentration and blood pressure. The alpha-2 agonist, BHT 933 (50 micrograms) and the beta agonist, isoproterenol (10 micrograms) both caused a significant decrease in the plasma vasopressin concentration with only small changes in blood pressure. The central administration of the alpha-1 antagonist corynanthine (20 micrograms) had no effect on the plasma vasopressin concentration; however, increases in plasma vasopressin levels were observed when either the alpha-2 antagonist yohimbine (20 micrograms) or the beta antagonist propranolol (20 micrograms) were given. It is concluded that central noradrenergic pathways may play an important role in the control of vasopressin release and that this control may involve alpha-1, alpha-2 and beta adrenoreceptors.

Animals↗

PubMed1987

Noradrenaline, by activation of alpha-1-adrenoceptors in the region of the supraoptic nucleus, causes secretion of vasopressin in the unanaesthetized rat.

In unanaesthetized rats chronically prepared with venous and intracerebral cannulae, noradrenaline injected into the region of the supraoptic nuclei caused a dose-dependent increase in plasma vasopressin, measured by radioimmunoassay. A similar response was obtained with phenylephrine, but not with either clonidine or isoprenaline. The secretion of vasopressin was not secondary to change in arterial pressure, since similar injections of noradrenaline resulted in a small increase in arterial pressure, measured in the anaesthetized rat. These results suggest that noradrenaline stimulates alpha-1-adrenoceptors, presumably located on vasopressin-secreting neurones, thereby causing these cells to secrete vasopressin into the circulation. Tyramine injections also resulted in a prompt elevation in plasma vasopressin, indicating that endogenous noradrenaline is capable of releasing vasopressin.

Animals↗

PubMed1988

Opioid-noradrenergic interactions in the neurohypophysis. I. Differential opioid receptor regulation of oxytocin, vasopressin, and noradrenaline release.

The actions of opioids on electrically evoked release of oxytocin, vasopressin, and noradrenaline-using the [3H]-noradrenaline technique-from the rat neurohypophysis were examined in vitro. Antagonism of the action of endogenous neurohypophysial opioids with naloxone enhanced release of peptides and [3H]-noradrenaline differentially. Naloxone enhanced oxytocin release by 100 and 173% in two series of experiments (ED50 7 x 10(-7) M), whilst vasopressin release was enhanced by only 30 and 20%, respectively. [3H]-noradrenaline release was maximally enhanced by 41% (ED50 2 x 10(-7) M). We examined the opioid receptor subtypes mediating these effects using selective receptor agonists. The kappa-agonist U-50,488H inhibited oxytocin and vasopressin release to a similar extent, but did not modify [3H]-noradrenaline release. The effects of U-50,488H were completely prevented by a tenfold molar excess of naloxone. The mu-agonist (D-Ala2, MePhe5 Gly-ol)-enkephalin also failed to inhibit [3H]-noradrenaline release and caused only a minor inhibition of oxytocin and vasopressin secretion. The delta-agonist (D-Pen2, D-Pen5)-enkephalin was without effect. We conclude that (1) kappa-receptors sensitive to U-50,488H mediate opioid inhibition of secretion from oxytocin and vasopressin nerve terminals; (2) when opioid actions are blocked by naloxone, opioid peptides within the neurohypophysis are shown to exert a much greater influence over oxytocin compared to vasopressin terminals; (3) neurohypophysial opioids also regulate release from noradrenergic terminals, although the nature of the receptors involved remains unclear, and (4) kappa-receptors can mediate inhibition of neurohormone secretion by an action independent of the neurohypophysial noradrenergic innervation.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

PubMed1993

Effect of serotonin on vasopressin release: a comparison to corticosterone, prolactin and renin.

Previously we reported that 5 min after intracerebroventricular (i.c.v.) injection, serotonin (5-HT, 2.5 micrograms) produced increases in blood pressure and decreases in heart rate in conscious rats that were blocked by LY 53857 (a selective 5-HT2/1C antagonist) and were sensitive to vasopressin antagonism. The present studies were performed to determine if this dose of 5-HT acts similarly to increase plasma vasopressin levels. In addition, the vasopressin responses were compared to prolactin, corticosterone, and plasma renin activity, three other neuroendocrine systems regulated in part by 5-HT. The administration of 5-HT (2.5 micrograms i.c.v.) produced a rapid (maximum response in less than 5 min) and brief (return to baseline by 15 min) increase in plasma vasopressin levels. The response was eliminated by the centrally acting 5-HT2/1C antagonist LY 53857 (100 micrograms/kg i.v.), but only attenuated by xylamidine (100 micrograms/kg i.v.), a 5-HT2/1C antagonist that reportedly does not cross the blood-brain barrier. 5-HT also increased plasma prolactin and corticosterone levels, but neither LY 53857 nor xylamidine altered these responses. In rats rendered chronically baroreceptor deficient by sinoaortic deafferentation, the vasopressin response to 5-HT was reduced, whereas the prolactin response was normal. 5-HT did not increase plasma renin activity in intact or baroreceptor-deficient rats, in contrast to the other neuroendocrine systems studied. Thus, the data demonstrate that vasopressin levels are elevated briefly following 5-HT i.c.v., consistent with the pharmacologic profile of the early cardiovascular response.(ABSTRACT TRUNCATED AT 250 WORDS)

Amidines↗

PubMed1980

Alpha-adrenergic blocking agents and the cardiovascular response to pharmacological doses of vasopressin.

The effects of alpha-adrenergic blockade with phentolamine or dibenamine on the cardiovascular response to pharmacological doses of vasopressin were studied in anesthetized dogs. Some observations were also made on the combined effects of vasopressin and norepinephrine. Changes in mean systemic arterial pressure, portal pressure, and resistance in the prehepatic splanchnic vasculature during vasopressin infusion were noted. A total of 97 dogs were used. alpha-Blockade appeared to enhance the response of arterial pressure to vasopressin, possibly because of loss of baroreceptor-mediated buffering action which normally attenuates its pressor action. Effects of vasopressin on mesenteric vascular resistance and portal pressure were unchanged or somewhat less after alpha-blockade, hence no evidence that its therapeutic effect would be improved by this combination. Vasopressin and norepinephrine when given together result in an additive pressor response with little or no evidence of potentiation.

Adrenergic alpha-Antagonists↗

PubMed1979

Plasma vasopressin variation and renin activity in normal active humans.

Plasma concentrations of vasopressin and plasma renin activity were measured every 30 min for 24 h in 5 normal active humans, in 1 normal woman confined to bed (except for brief periods up to the bathroom), in 2 active patients with primary aldosteronism and in 1 patient with low-renin hypertension. Plasma vasopressin varied markedly over the day and night in a pattern suggesting episodic secretion of the hormone in the normal subjects. Assumption of upright posture was accompanied by a rise in plasma levels from undetectable to 20--50 pg/ml. Episodic secretion, however, also occurred during bed rest and sleep. In contrast, patients with primary aldosteronism and low-renin hypertension had plasma vasopressin levels considerably lower than the normals, and their profiles of plasma concentration lacked the peaks seen in normals. In the normals, although vasopressin and renin secretion often coincided, only 2 of 6 studies showed a significant correlation between the plasma levels of the two hormones. This study, therefore, shows that vasopressin is secreted periodically in normal humans, that upright posture is an important modulator of secretory activity and that the renin-angiotensin system may or may not influence the pattern of secretion. In addition, it underlines the necessity of recumbency in establishing the existence of a circadian rhythm of plasma vasopressin levels.

Adult↗

PubMed1999

Reversal by vasopressin of intractable hypotension in the late phase of hemorrhagic shock.

BACKGROUND: Hypovolemic shock of marked severity and duration may progress to cardiovascular collapse unresponsive to volume replacement and drug intervention. On the basis of clinical observations, we investigated the action of vasopressin in an animal model of this condition. METHODS AND RESULTS: In 7 dogs, prolonged hemorrhagic shock (mean arterial pressure [MAP] of approximately 40 mm Hg) was induced by exsanguination into a reservoir. After approximately 30 minutes, progressive reinfusion was needed to maintain MAP at approximately 40 mm Hg, and by approximately 1 hour, despite complete restoration of blood volume, the administration of norepinephrine approximately 3 micrograms . kg(-1). min(-1) was required to maintain this pressure. At this moment, administration of vasopressin 1 to 4 mU. kg(-1). min(-1) increased MAP from 39+/-6 to 128+/-9 mm Hg (P<0.001), primarily because of peripheral vasoconstriction. In 3 dogs subjected to similar prolonged hemorrhagic shock, angiotensin II 180 ng. kg(-1). min(-1) had only a marginal effect on MAP (45+/-12 to 49+/-15 mm Hg). Plasma vasopressin was markedly elevated during acute hemorrhage but fell from 319+/-66 to 29+/-9 pg/mL before administration of vasopressin (P<0.01). CONCLUSIONS: Vasopressin is a uniquely effective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and catecholamine vasopressors. Vasopressin deficiency may contribute to the pathogenesis of this condition.

Adult↗

PubMed1989

Baroreceptor influences on oxytocin and vasopressin secretion.

The objective of these studies was to investigate the role of arterial baroreceptors in the control of neurohypophyseal secretion. The effect of sinoaortic denervation on basal and osmotic-induced release of oxytocin and vasopressin and on blood pressure was determined. Hypertonic or isotonic saline was infused intravenously into sham-operated or denervated rats 3 days after surgery. Plasma oxytocin and vasopressin were measured at 5 and 15 minutes after the infusion. The control levels of oxytocin were increased in the denervated rats, but vasopressin levels were not significantly altered. The vasopressin and oxytocin responses to hypertonic saline were greater after baroreceptor denervation. Plasma oxytocin was increased from 4.7 +/- 0.9 to 72.2 +/- 8.7 pg/ml in the denervated rats and from 1.8 +/- 0.3 to 39.9 +/- 6.7 pg/ml in the sham-operated control group at 5 minutes after the infusion (p less than 0.01). The plasma vasopressin response to hypertonic saline was 7.1 +/- 0.6 pg/ml in the sham-operated versus 11.1 +/- 1.6 pg/ml in the denervated rats (p less than 0.05). There was no difference between sham-operated and denervated rats in the effect of hypertonic saline on plasma sodium and hematocrit. Mean arterial blood pressure was increased after sinoaortic denervation (116.3 +/- 4.2 mm Hg in the sham-operated vs. 138.2 +/- 8.3 mm Hg in the denervated rats, p less than 0.05); however, there was no difference in the pressor response to hypertonic saline. These results show that the baroreceptor system influences the secretion of both oxytocin and vasopressin, with effects on basal secretion as well as the response to an osmotic stimulus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗