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PubMed1989

A1 cell group mediates solitary nucleus excitation of supraoptic vasopressin cells.

Stimulation of the nucleus tractus solitarius (NTS) excites putative vasopressin-secreting cells of the supraoptic nucleus (SON) via a catecholaminergic projection to hypothalamus. Despite recent evidence of a direct catecholaminergic projection from NTS to SON, we have performed single-unit recording experiments in pentobarbital sodium-anesthetized rats to investigate the possibility that NTS stimulation effects on SON vasopressin cells are indirect, being relayed via the A1 noradrenergic cell group of the caudal ventrolateral medulla. The effects of single-pulse NTS and A1 region stimulation on the activity of antidromically identified SON neurosecretory cells that had been functionally characterized as vasopressin secreting were compared. NTS stimulation excited 81% of all putative vasopressin-secreting cells tested (n = 83), with a mean onset latency of 51 +/- 1 ms. A1 region stimulation excited 76% of all cells tested and 90% of units responsive to NTS stimulation, with a mean latency of 39 +/- 1 ms. Consistent with previous work NTS stimulation excited only a minority of oxytocin cells tested (3/13), and of these two-thirds also responded to A1 stimulation. Bilateral electrolytic lesions of the A1 region abolished the effects of NTS stimulation on putative vasopressin cells. Ipsilateral A1 region injections of the inhibitory neurotransmitter gamma-amino-butyric acid reversibly blocked NTS stimulation effects on putative vasopressin cells in animals where the contralateral A1 region had already been lesioned. These results support the proposal that excitation of SON vasopressin-secreting cells after NTS stimulation is due to activation of a relay projection through the A1 noradrenergic cell group of the caudal ventrolateral medulla.

Animals↗
PubMed2002

Role of the cytoskeleton in mediating effect of vasopressin and herbimycin A on secretory K channels in CCD.

We have previously demonstrated that inhibiting protein tyrosine kinase (PTK) and stimulating protein kinase A (PKA) increase the activity of the small-conductance K (SK) channel in the cortical collecting duct (CCD) of rat kidneys (Cassola AC, Giebisch G, and Wang WH. Am J Physiol Renal Fluid Electrolyte Physiol 264: F502-F509, 1993; Wang WH, Lerea KM, Chan M, and Giebisch G. Am J Physiol Renal Physiol 278: F165-F171, 2000). In the present study, we used the patch-clamp technique to study the role of the cytoskeleton in mediating the effect of herbimycin A, an inhibitor of PTK, and vasopressin on the SK channels in the CCD. The addition of colchicine, an inhibitor of microtubule assembly, or taxol, an agent that blocks microtubule reconstruction, had no significant effect on channel activity. However, colchicine and taxol treatment completely abolished the stimulatory effect of herbimycin A on the SK channels in the CCD. Removal of the microtubule inhibitors restored the stimulatory effect of herbimycin A. In contrast, treatment of the tubules with either taxol or colchicine did not block the stimulatory effect of vasopressin on the SK channels. Moreover, the effect of herbimycin A on the SK channels was also absent in the CCDs treated with either cytochalasin D or phalloidin. In contrast, the stimulatory effect of vasopressin was still observed in the tubules treated with phalloidin. However, cytochalasin D treatment abolished the effect of vasopressin on the SK channels. Finally, the effects of vasopressin and herbimycin A are additive because inhibiting PTK can still increase the channel activity in CCD that has been challenged by vasopressin. We conclude that an intact cytoskeleton is required for the effect on the SK channels of inhibiting PTK and that the SK channels that are activated by inhibiting PTK were differently regulated from those stimulated by vasopressin.

Actins↗
PubMed2002

Vasopressin rapidly increases phosphorylation of UT-A1 urea transporter in rat IMCDs through PKA.

The UT-A1 urea transporter plays an important role in maintaining the hyperosmolar milieu of the inner medulla. Vasopressin increases urea permeability in rat terminal inner medullary collecting ducts (IMCDs) within 5-10 min. To elucidate the mechanism, IMCD suspensions were radiolabeled with [(32)P]orthophosphate. UT-A1 was immunoprecipitated and analyzed by autoradiogram and Western blot. Both the 97- and 117-kDa UT-A1 proteins were phosphorylated. Vasopressin treatment increased the phosphorylation of both UT-A1 proteins at 2 min, which peaked at 5-10 min and remained elevated for up to 30 min. There was a discernable increase in UT-A1 phosphorylation with 10 pM and a 50% increase with 10-100 nM vasopressin. 1-Desamino-8-D-arginine vasopressin (dDAVP) or 8-(4-chlorophenylthio)-cAMP (CPT-cAMP) also increased UT-A1 phosphorylation. The vasopressin-stimulated increase in UT-A1 phosphorylation was blocked by H-89 or a specific peptide inhibitor of protein kinase A. Phosphatase inhibitors (okadaic acid, calyculin) increased UT-A1 phosphorylation. We conclude that vasopressin increases UT-A1 phosphorylation via protein kinase A within 2-5 min in rat IMCDs. This suggests that phosphorylation of UT-A1 may be the mechanism by which vasopressin rapidly increases urea permeability in vivo.

Animals↗
PubMed1988

Protein synthesis inhibitors attenuate water flow in vasopressin-stimulated toad urinary bladder.

Vasopressin stimulates the introduction of aggregated particles, which may represent pathways for water flow, into the luminal membrane of toad urinary bladder. It is not known whether water transport pathways are degraded on removal from membrane or whether they are recycled. We examined the effect of the protein synthesis inhibitors cycloheximide and puromycin using repeated 30-min cycles of vasopressin followed by washout of vasopressin, all in the presence of an osmotic gradient, a protocol that maximizes aggregate turnover. "High dose" cycloheximide (200 micrograms/ml) inhibited flow immediately. "Low dose" cycloheximide (1 microgram/ml) did not affect initial flow; however, flow was inhibited by the fourth restimulation. On further rechallenge, inhibition persisted but did not increase. In the absence of vasopressin, inhibition did not develop. Despite the inhibition of flow in vasopressin-treated tissues, the cAMP-dependent protein kinase ratio (-cAMP/+cAMP), an index of in vivo cAMP effect, was elevated in cycloheximide-treated tissues, suggesting modulation at a distal site in the stimulatory cascade. Cycloheximide inhibited flow when 10 microM forskolin or 0.2 mM 8-BrcAMP was substituted for vasopressin in the fourth period; however, MIX (4 mM)-stimulated flow was enhanced by 1 microgram/ml cycloheximide but inhibited by 200 micrograms/ml cycloheximide. [14C]urea permeability was not inhibited by cycloheximide. Puromycin (0.5 mM) also inhibited water flow by the fourth challenge with vasopressin. The data suggest that protein synthesis inhibitors attenuate flow at a site that is distal to cAMP-dependent protein kinase.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1992

Kinetics of urea and water permeability activation by vasopressin in rat terminal IMCD.

The vasopressin-regulated urea carrier and the vasopressin-regulated water channel are distinct transporters present in the apical membrane of the inner medullary collecting duct (IMCD) cells. To assess whether these transporters may be activated by common mechanisms, we investigated the time course of increase of urea and water permeability in response to vasopressin in isolated perfused terminal IMCD segments. The permeability responses were determined through the use of a specially designed continuous-flow fluorometer for rapid analysis of collected tubule fluid samples. The time courses of activation of the two transporters by vasopressin were virtually identical. Both urea and water permeability displayed a rapid initial increase for the first 10 min followed by a slower secondary response lasting at least 30 additional min. The lag periods between vasopressin addition and the initial rise in permeability were the same for urea (34.2 +/- 8.8 s) and water (34.8 +/- 8.9 s) transport activation. Furthermore, the initial rate of permeability increase (normalized by the total increase) was not significantly different for the two transport processes. The lag periods for the increase in urea permeability in response to 8-bromoadenosine 3',5'-cyclic monophosphate and vasopressin were not significantly different. The results are consistent with the view that the rate-limiting step in vasopressin-induced activation is the same for both the urea carrier and water channel and may lie at a step beyond generation of adenosine 3',5'-cyclic monophosphate.

Animals↗
PubMed1993

Hypertonic sucrose treatment enhances second messenger accumulation in vasopressin-sensitive cells.

When we treated vasopressin-sensitive vascular smooth muscle cells (A10 cells) and kidney cells (LLC-PK1 cells) with hypertonic sucrose and vasopressin, we observed a decrease in the internalization of radiolabeled vasopressin into these cells and an increase in the amount of second messenger present in these cells following vasopressin stimulation. In A10 cells exposed to hypertonic sucrose, there was an increase in the amount of cellular inositol phosphates accumulated in response to vasopressin compared with cells not exposed to hypertonic sucrose. Similarly, in hypertonic sucrose-treated LLC-PK1 cells, vasopressin increased the amount of adenosine 3',5'-cyclic monophosphate (cAMP) present within the cells compared with LLC-PK1 cells not exposed to hypertonic sucrose. Hypertonic sucrose treatment inhibited receptor-mediated endocytosis in both these cell lines. Hypertonic sucrose alone did not increase the basal amounts of inositol phosphates or cAMP present in A10 or LLC-PK1 cells, respectively. Hypertonic sucrose treatment inhibits receptor endocytosis and increases second messenger concentrations in vasopressin-sensitive cells.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Angiotensin II increases vasopressin-stimulated facilitated urea permeability in rat terminal IMCDs.

Angiotensin II receptors are present along the rat inner medullary collecting duct (IMCD), although their physiological role is unknown. Because urea is one of the major solutes transported across the terminal IMCD, we measured angiotensin II's effect on urea permeability. In the perfused rat terminal IMCD, angiotensin II had no effect on basal urea permeability but significantly increased vasopressin-stimulated urea permeability by 55%. Angiotensin II, both without and with vasopressin, also increased the amount of (32)P incorporated into urea transporter (UT)-A1 in inner medullary tissue exposed to these hormones ex vivo. Because angiotensin II activates protein kinase C, we tested the effect of staurosporine (SSP). In the absence of angiotensin II, SSP had no effect on vasopressin-stimulated urea permeability in the perfused terminal IMCD. However, SSP completely and reversibly blocked the angiotensin II-mediated increase in vasopressin-stimulated urea permeability. SSP and chelerythrine reduced the angiotensin II-stimulated (32)P incorporation into UT-A1 in inner medullary tissue exposed ex vivo. We conclude that angiotensin II increases vasopressin-stimulated facilitated urea permeability and (32)P incorporation into the 97- and 117-kDa UT-A1 proteins via a protein kinase C-mediated signaling pathway. These data suggest that angiotensin II augments vasopressin-stimulated facilitated urea transport in the rat terminal IMCD and may play a physiological role in the urinary concentrating mechanism by augmenting the maximal response to vasopressin.

Angiotensin II↗
PubMed1981

Effects of vasopressin administration on diuresis of water immersion in normal humans.

Although previous studies have demonstrated that water immersion to the neck (NI) results in a significant diuresis, the mechanisms are incompletely delineated. Because recent studies in our laboratory have demonstrated that NI is associated with a suppression of antidiuretic hormone (ADH), it is possible that such a suppression mediates the encountered diuresis. The present study was undertaken to assess more directly the relative role of ADH suppression by determining the effects of vasopressin administration. Six hydrated normal subjects were studied on two occasions while undergoing 6 h of NI. During the second NI study, aqueous vasopressin (20 mU/h) was infused for the initial 4 h of study (NI + vasopressin). NI resulted in a significant increase in urinary flow rate beginning during hour 1 and persisting throughout NI. In contrast, during NI + vasopressin, the anticipated diuresis was abolished throughout the 4 h of vasopressin administration. Cessation of vasopressin administration during the final 2 h of NI + vasopressin resulted in a marked and prompt diuresis. The present observations are consistent with the formulation that ADH suppression participates importantly in mediating the diuresis of NI in hydrated normal subjects.

Adult↗
PubMed1999

PC18, a specific aminopeptidase N inhibitor, induces vasopressin release by increasing the half-life of brain angiotensin III.

Angiotensin III (AngIII), which is metabolized in vivo by aminopeptidase N (APN), was previously shown to be one of the main effector peptides of the brain renin-angiotensin system (RAS) in the control of vasopressin release. Recently, a potent APN inhibitor, PC18 (2-amino-4-methylsulfonyl butane thiol, methionine thiol), has been developed. In this study, we first checked the in vitro selectivity of PC18 towards APN, aminopeptidase A (APA) and aminopeptidase B (APB), three zinc metalloproteases with significant identity between their amino acid sequences. The Ki values of this compound on APN were found to be in the nanomolar range (Ki = 8.0 +/- 1.7 nM) but it was 2,150 and 125 times less active on APA and APB, respectively. Secondly, we evaluated in vivo the effect of brain APN inhibition with PC18 on the inactivation of brain AngIII and on vasopressin secretion in mice. For this purpose, mice received [3H]AngII intracerebroventricularly in the presence or absence of the APN inhibitor PC18 (30 microg). At different times after the injection, [3H]AngIII levels were evaluated from hypothalamus homogenates after separation by cation-exchange chromatography. PC18 induced an accumulation of [3H]AngIII, increasing its half-life 3.9 times as compared with control values. In addition, the effect of PC18 on vasopressin release was studied in mice. PC18 (10-100 microgram) was injected intracerebroventricularly, and plasma vasopressin levels were estimated by radioimmunoassay. PC18 increased vasopressin levels in a dose-dependent manner. The maximal increase in vasopressin release (+220%) is observed for a dose of PC18 of 100 microgram and was inhibited 75% by the coadministration of the AngII receptor antagonist (Sar1-Ala8)-AngII (0.5 microgram). These results indicate that in vivo, in the mouse brain, APN inhibition by PC18 increases the half-life of endogenous AngIII, resulting in an enhanced vasopressin release.

Aminopeptidases↗
PubMed2004

Oxytocin and vasopressin immunoreactivity within the forebrain and limbic-related areas in the mustached bat, Pteronotus parnellii.

The nonapeptides, oxytocin and arginine vasopressin, play an important role in mammalian social and reproductive behavior. Using immunocytochemical procedures, we identified oxytocin-immunoreactive neurons in the frontal and auditory cortices, limbic areas such as the medial septal nucleus, horizontal limb of the diagonal band and the amygdala. Only arginine vasopressin neurons were present in the bed nucleus of the stria terminalis. In limbic-related areas, the hypothalamic paraventricular and supraoptic nuclei and the nucleus centralis contained both oxytocin and arginine vasopressin neurons. The medial preoptic area showed a positive reaction for several arginine vasopressin fibers, but not oxytocin fibers, except in one female bat sacrificed during the breeding season. Arginine vasopressin fibers were observed in another limbic-related area, the periaqueductal gray. Furthermore, oxytocin was predominantly localized within sensory (e.g., auditory) and frontal cortex and limbic areas, whereas arginine vasopressin was restricted largely to known audiovocal regions of the periaqueductal gray. Classical neurosecretory nuclei in the hypothalamus contain both peptides. Oxytocin-immunoreactive neurons were also found in other structures such as the olfactory bulb, olfactory tubercle, primary and secondary motor cortex, fronto-parietal cortex, piriform cortex and the nucleus of the internal capsule. Both oxytocin and arginine vasopressin immunoreactivity was present in the suprachiasmatic nucleus, median eminence, neural lobe of the hypophysis and the pineal gland. Together with previous studies, the presence of these peptides within auditory areas of the cortex (sensory and frontal), and limbic as well as limbic-related regions provides anatomical evidence supporting their proposed role in social vocal behaviors and probably in auditory processing.

Animals↗
PubMed1983

Vasopressin and oxytocin content are decreased in the brain stems of spontaneously hypertensive rats.

The brain stem and neurohypophyseal content of arginine vasopressin and the brain stem content of oxytocin were measured by radioimmunoassay in 3-, 7-, and 22- to 28-week-old spontaneously hypertensive rats of the stroke-prone strain (SHRSP) and the values were compared to those measured in age-matched normotensive Wistar-Kyoto rats (WKY). When compared to WKY, the content of vasopressin in the brain stems of SHRSP was reduced in all three age-groups; in contrast, the neurohypophyseal contents of vasopressin in the two species were not significantly different at 3 and 7 weeks of age and the content was increased slightly in SHRSP at 22-28 weeks. Similar to the findings for vasopressin in the brain stem, the content of oxytocin in this tissue was reduced in SHRSP at 7 and 22-28 weeks of age. The results demonstrate that brain stem arginine vasopressin levels and neurohypophyseal arginine vasopressin levels may change differentially and that the age-related differences in the brain stem levels of arginine vasopressin and oxytocin in SHRSP and WKY are consistent with the possibility that these peptides may play a role in altering cardiovascular reflex activity.

Age Factors↗
PubMed1984

GABA agonists inhibit the vasopressin-dependent pressor effects of central angiotensin II.

Previous studies have demonstrated that intraventricular (IVT) administration of low doses of gamma-aminobutyric acid (GABA) agonists reduced the pressor effects of centrally injected angiotensin II (AII). The following studies were designed to determine if GABA agonists acted to inhibit the pressor response of AII through blockade of the vasopressin-dependent pressor component. Following pretreatment with a vascular vasopressin antagonist, the pressor response of IVT administered AII was reduced approximately 50%. Hypophysectomy produced a similar reduction in this pressor response. These results suggested that vasopressin contributed to one-half of the pressor response of AII. In order to generate a vasopressin-dependent response, the sympathetic nervous system was eliminated with ganglionic blockade by chlorisondamine. The increase in arterial pressure produced by IVT injected AII after ganglionic blockade was augmented compared to untreated rats. This potentiated pressor effect of IVT administered AII after chlorisondamine treatment was markedly reduced by a vascular vasopressin antagonist or by hypophysectomy. Therefore, the pressor effect of AII after ganglionic blockade was caused principally by the pressor actions of arginine-vasopressin (AVP). This AVP-dependent pressor effect of IVT injected AII was reduced by pretreatment with 100 micrograms of GABA or 50 ng of the GABA agonist muscimol. These doses of GABA and muscimol have previously been shown to reduce the pressor response of IVT administered AII by approximately 60% in untreated rats. Thus, pretreatment with low doses of GABA agonists reduced the pressor effect of IVT injected AII in part by inhibiting the vasopressin component of this response.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed1986

Naloxone does not improve cardiovascular or blunt vasopressin responses in spontaneously hypertensive rats following graded hemorrhage.

The effects of continuous intravenous infusion of naloxone or vehicle on the blood pressure and vasopressin responses to step-wise hemorrhage were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Step-wise hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. The WKY were relatively resistant to the hypotensive effect of hemorrhage. No significant differences were noted in blood pressure responses between naloxone-treated and vehicle-treated SHR while naloxone treatment attenuated hypotension only slightly in WKY. Plasma vasopressin levels were also elevated by naloxone treatment in SHR following a nonhypotensive hemorrhage equivalent to 0.5% of body weight. However, no differences were observed between plasma vasopressin levels in naloxone-treated and vehicle-treated SHR at greater degrees of hemorrhage. In addition, plasma vasopressin levels were similar at all times in hemorrhaged WKY, regardless of treatment. Plasma vasopressin levels were increased by naloxone in both time-control SHR and WKY. The data demonstrate that naloxone-sensitive systems exert only minimal effects on the immediate cardiovascular responses to hypovolemia in normotensive rats and no measurable effects in SHR. It does appear that naloxone-sensitive mechanisms contribute a small, but significant, tonic inhibitory influence over vasopressin secretion in both normotensive and hypertensive rats under basal conditions and in SHR in response to a small reduction in blood volume.

Animals↗
PubMed1988

Neuropharmacological characterization of serotoninergic stimulation of vasopressin secretion in conscious rats.

In this study we have evaluated a possible role for brain serotoninergic neurons in the regulation of vasopressin secretion using pharmacological methods. In order to accomplish this, we have developed a specific and sensitive vasopressin radioimmunoassay along with a highly reproducible plasma extraction protocol. These tools were used to evaluate the plasma vasopressin response to several pharmacological challenges in conscious rats. Treatment with the serotonin (5-HT) releaser p-chloroamphetamine caused a significant increase in plasma vasopressin concentration. This effect was blocked by posterior hypothalamic deafferentation which separates serotonin cell bodies in the midbrain from their nerve terminals in the hypothalamus. Administration of graded doses of several 5-HT agonists had no effect. However, treatment with MK212, a serotonin agonist with 5-HT1 + 5-HT2 activity, induced a significant increase in plasma vasopressin concentration. The effect of MK212 on plasma vasopressin was completely abolished by the selective 5-HT2 receptor blocker LY53857. These studies confirm and extend studies by others that provide pharmacological evidence for serotoninergic regulation of vasopressin secretion via a selective 5-HT2 receptor mechanism. The specific neuroanatomical site(s) where serotonin exerts this effect are unknown, and the physiological consequences of these studies remain to be established.

Amphetamines↗
PubMed1991

Muscarinic cholinergic control of vasopressin secretion from the acute hypothalamoneurohypophysial explant.

Much of the afferent input thought to modulate vasopressin release from the magnocellular neuroendocrine cells of the supraoptic nucleus terminates in the region dorsal to the supraoptic nucleus. Cholinergic cells within this region may participate in the local processing of these afferent signals via synapses onto muscarinic cholinergic receptors. To investigate the role of these local synapses in vasopressin secretion, we characterized the muscarinic cholinergic influence on vasopressin secretion from the acute hypothalamoneurohypophysial explant in vitro. Acetylcholine induced a small dose-related secretion of vasopressin which could be totally blocked by atropine but not the nicotinic cholinergic antagonist, hexamethonium. Nicotine failed to release vasopressin from the explant, whereas alpha-bungarotoxin elicited a hypothalamic release of vasopressin which was atropine insensitive. Thus, local muscarinic receptors in the hypothalamus appear to participate in the control of neurohypophysial vasopressin secretion. The small magnitude of effect, however, is consistent with an indirect modulatory role rather than a major driving force for activation of the magnocellular neurons.

Acetylcholine↗
PubMed1993

Evidence that nitric oxide can act centrally to stimulate vasopressin release.

Nitric oxide (NO) is the endothelium-derived relaxing factor, which causes relaxation of vascular smooth muscle. NO synthetase, the enzyme for the synthesis of NO from its precursor L-arginine, is also widely distributed in neurons in the brain, and it has been suggested that NO may serve as an important neuromodulator. Because NO synthetase is present in the hypothalamus in relatively high concentration, we have determined whether NO can affect the release of vasopressin in conscious, chronically prepared rats. The intracerebroventricular (i.c.v.) injection of S-nitroso-N-acetylpenicillamine (12.5 and 25 micrograms; SNAP), that spontaneously breaks down to form NO, caused transient dose-related increases in the plasma vasopressin concentration of 1 and 2 microU/ml (p < 0.01), respectively. In control experiments in which N-acetylpenicillamine (25 micrograms), the precursor for the preparation of SNAP, was injected i.c.v. there was a small, 0.4 microU/ml, increase (p < 0.01) in the plasma vasopressin level. The i.c.v. injection of L-arginine (0.5 and 1 mg), also the precursor for the biosynthesis of NO, resulted in dose-dependent increases in the plasma vasopressin concentration similar in magnitude to those caused by SNAP. When D-arginine (1 mg), which cannot serve as a substrate for NO synthetase, was injected i.c.v., there was only a slight delayed increase in the plasma vasopressin concentration. Thus, NO can act centrally to stimulate vasopressin release and may serve as a neuromodulator in the control of vasopressin release.

Animals↗
PubMed1993

GABA-A agonist muscimol inhibits stimulated vasopressin release in the posterior pituitary of Sprague-Dawley, Wistar, Wistar-Kyoto and spontaneously hypertensive rats.

Vasopressin-containing neurosecretory cells are partly regulated by GABAergic neurons present both at the hypothalamic and the pituitary level. In the present work, we compared GABA effects on vasopressin release from posterior pituitaries of Sprague-Dawley (SPD), Wistar (W), Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Release of vasopressin was studied in vitro by placing neurointermediate lobes in perfusion chambers. It was stimulated twice by 50 mM KCl (S1 and S2) and the ratio between the first and the second stimulation was calculated (S2/S1). The basal and stimulated release of vasopressin was enhanced in the SHR. There was no difference in vasopressin content in the pituitary between the WKY and the SHR but the levels were lower compared to the SPD rat. Muscimol, a GABA-A receptor agonist, was added during S2. Muscimol inhibited in a dose-dependent manner the stimulated release of vasopressin, with an ED50 about 3 microM. The effect of muscimol was not statistically different between the strains expressed in ratios. The actual inhibition was apparently greater in the SHR, as both basal and stimulated vasopressin release was larger.

Animals↗
PubMed1989

Vasopressin and the mature coronary collateral circulation.

In isolated vascular rings, we have shown that mature coronary collateral vessels are highly responsive to the vasoconstrictor effects of vasopressin. The purpose of the present study was to determine the effect of concentrations of vasopressin encountered in pathophysiologic states on the collateral circulation in vivo. We studied eight open-chest anesthetized dogs with mature coronary collateral vessels 3-6 months after placement of an ameroid constrictor on the left circumflex coronary artery. The left anterior descending coronary artery was perfused at constant pressure, and peripheral coronary pressure was monitored continuously throughout each experiment. At baseline and during intracoronary infusion of vasopressin, which resulted in concentrations ranging from 8 +/- 3 to 1,340 +/- 327 microM/ml, we measured regional myocardial perfusion with radiolabeled microspheres. At baseline, regional myocardial perfusion to the collateral-dependent myocardium and to the normally perfused myocardium was similar; however, during vasopressin infusion, collateral-dependent zone flow decreased by 49 +/- 14% whereas normal zone flow decreased by only 9 +/- 9% (p less than 0.0005, normal zone perfusion vs. collateral perfusion). Vasopressin increased transcollateral resistance by 242 +/- 95% above baseline but produced a more modest increase in normal zone resistance (15 +/- 10%). The subendocardial to subepicardial perfusion ratio increased by 28 +/- 12% in the normal zone in response to vasopressin but decreased by 18 +/- 11% in the collateral-dependent zone. These data show that mature coronary collateral vessels are responsive to the vasoconstrictor effects of vasopressin at concentrations encountered in various pathophysiologic states.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗