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PubMed2000

Vasopressin and thirst in patients with posterior pituitary ectopia and hypopituitarism.

OBJECTIVE: Partial diabetes insipidus has been documented in patients with congenital hypopituitarism and posterior pituitary ectopia, some cases being clinically silent except for enuresis. The objective of our study was to evaluate vasopressin (AVP) secretion and thirst appreciation in hypopituitary patients with posterior pituitary ectopia. PATIENTS: Twelve males and three females, aged between 13 and 38 years (median 19 years). Eleven had multiple pituitary deficiencies, adequately replaced at the time of the study, and four were only growth hormone deficient. None of the patients suffered from polyuria, polydipsia or nocturnal enuresis. We tested the patients with a 5% NaCl infusion. Five patients with abnormal vasopressin production were also tested with nitroprusside, which affects baroceptor vasopressin secretion. RESULTS: We found that only two out of 12 patients had normal AVP secretion. Thirst assessment showed severe hypodipsia in one patient, hyperdipsia in three out of 15 and more subtle abnormalities in two out of 15 patients. Concordance was found between osmotically and baroceptor-stimulated vasopressin. CONCLUSIONS: Patients with posterior pituitary ectopia showed a high prevalence of subclinical subnormal vasopressin response to the osmolar stimulus and moreover an impairment of thirst appreciation. Our data on nonosmotically stimulated AVP release suggest the existence of a damage in the hypothalamic vasopressin secreting centres.

Adolescent↗

PubMed2002

Effects of long-term octreotide treatment on the response of portal-systemic collaterals to vasopressin in portal hypertensive rats.

BACKGROUND: Chronic portal hypertension is associated with the development of portal-systemic collaterals. Long-term octreotide treatment has been shown to enhance the constrictive response to vasopressin in the mesenteric arteries of portal hypertensive rats. This study investigated the effects of long-term octreotide treatment on the response of portal-systemic collaterals to vasopressin in portal hypertensive rats. METHODS: Partially portal vein-ligated rats were divided into two groups to receive subcutaneous injection of either placebo (5% dextrose in water) or octreotide (30 microg kg(-1)) twice daily for 7 days. Two series of experiments were performed to measure: (a) the systemic and portal hemodynamics and cumulative concentration-response curves of collateral vessels to vasopressin (10(-10) to 10(-7 )M) and (b) the slopes of the flow-pressure curves of collaterals (an index of portal-systemic shunting). The cumulative concentration-response curves and flow pressure curves were determined by the in situ collateral perfusion. RESULTS: Long-term octreotide treatment significantly lowered the portal pressure without changes in the mean arterial pressure. Vasopressin significantly and similarly increased the perfusion pressure of collateral vessels in both the placebo- and octreotide-treated groups. In addition, long-term octreotide treatment exerted no effect on the EC(50) of vasopressin (-8.25 +/- 0.19 vs. -8.20 +/- 0.10, P > 0.05) and the slopes of flow-pressure curves (0.97 +/- 0.02 vs. 0.94 +/- 0.04, P > 0.05) in the collaterals. CONCLUSION: Despite lowering the portal pressure, long-term octreotide treatment did not enhance the vasoconstrictive effect of vasopressin in the collateral vessels of portal hypertensive rats and ameliorate the degree of portal-systemic shunting.

Animals↗

PubMed2000

Gonadotropin-releasing hormone exhibits circadian rhythm in phase with arginine-vasopressin in co-cultures of the female rat preoptic area and suprachiasmatic nucleus.

To determine whether the suprachiasmatic nucleus can drive a circadian release of gonadotropin-releasing hormone (GnRH) in the preoptic area, we measured the release of GnRH, arginine-vasopressin and vasoactive intestinal polypeptide (VIP) in cocultures of the preoptic area and the suprachiasmatic nucleus at 2-h intervals over a period of 120 h. The release of GnRH in cocultures exhibited a significant circadian rhythm in the presence of oestrogen but not in the absence of oestrogen. The period of the GnRH circadian rhythm was the same as that of the arginine-vasopressin circadian rhythm, and different from the VIP circadian rhythm in each coculture. Furthermore, the peak phase of the GnRH rhythm occurred at the time same as that of the arginine-vasopressin rhythm in each coculture. However, the peak phase of the GnRH rhythm was not always the same as that of the VIP rhythm. Administration of arginine-vasopressin significantly increased GnRH release in single preoptic area cultures in the presence of oestrogen, but VIP did not. The result suggests that, in cocultures of the suprachiasmatic nucleus and the preoptic area, arginine-vasopressin neurones drive the circadian release of GnRH in the presence of oestrogen. We suggest that arginine-vasopressin neurones in the suprachiasmatic nucleus mediate the clock information to GnRH neurones in vivo as well.

Animals↗

PubMed2002

Comparison of the efficacy of octreotide, vasopressin, and omeprazole in the control of acute bleeding in patients with portal hypertensive gastropathy: a controlled study.

BACKGROUND: Portal hypertensive gastropathy is an important complication of liver cirrhosis and it contributes to acute gastric bleeding. Effective management of this condition remains a clinical challenge. We assessed and compared the efficacy of octreotide, vasopressin, and omeprazole in the treatment of acute bleeding in patients with portal hypertensive gastropathy. METHODS: Sixty-eight patients with portal hypertensive gastropathy were randomized into Octreotide, Vasopressin, and Omeprazole groups. Bleeding was monitored by observing the contents of the nasogastric tube. Blood transfusion requirements and side-effects of drugs were recorded. Repeat endoscopies were scheduled 2 weeks after treatment. RESULTS: Complete bleeding control after 48 h of drug infusion was achieved in all patients receiving octreotide (100%), 14/22 patients receiving vasopressin (64%), and 13/22 patients receiving Omeprazole (59%). Octreotide required much less time and significantly fewer blood transfusions to control bleeding. Patients receiving vasopressin experienced more side-effects than those receiving octreotide and omeprazole. In the 17 patients whose bleeding was not controlled within 48 h by either vasopressin or omeprazole, complete bleeding control was achieved by combined use of these two agents. Follow-up endoscopy showed dramatic improvement in gastric mucosal erosions, superficial ulceration and erythema. CONCLUSIONS: Octreotide appeared to be more effective in controlling acute bleeding in patients with hypertensive gastropathy, with significantly rapid action, smaller transfusion requirements, and minor side-effects. Simultaneous administration of vasopressin and omeprazole appeared to have additive effects.

Adult↗

PubMed2003

Differential routing of coexisting neuropeptides in vasopressin neurons.

The functional implications of intraneuronal coexistence of different neuropeptides depend on their respective targeting to release sites. In the rat hypothalamic magnocellular neurons, we investigated a possible differential routing of the coexpressed galanin and vasopressin. The respective location of proteins and messengers was assessed with double immunogold and in situ hybridization combining confocal and electron microscope analysis. The various populations of labelled granules were quantitatively compared in three subcellular compartments: perikarya, local processes and posthypophyseal nerve endings. Three subpopulations of granules were detected in all three compartments, but their respective amount showed significant differences. Galanin alone was immunolocalized in some secretory granules, vasopressin alone in others, and both peptides in a third subpopulation of granules. The major part of the granules containing vasopressin, either alone or in association with galanin, is found in neurohypophyseal nerve endings. In contrast, galanin single-labelled granules represent the most abundant population in dendritic processes, while double-labelled granules are more numerous in perikarya. This indicates a preferential distribution of the two peptides in the different compartments of magnocellular neurons. Furthermore, galanin and vasopressin messenger RNAs were detected at different domains of the endoplasmic reticulum, suggesting that translation might also occur at different locations, thus leading to partial segregation of galanin and vasopressin cargoes between two populations of secretory granules. The present study provides, for the first time in mammals, evidence suggesting that galanin and vasopressin are only partly copackaged and undergo a preferential targeting toward dendrites or neurohypophysis, suggesting different functions, autocrine/paracrine and endocrine, respectively.

Animals↗

PubMed1981

Blood pressure in acute and chronic vasopressin excess: studies of malignant hypertension and the syndrome of inappropriate antidiuretic hormone secretion.

We studied 29 patients with malignant hypertension and 28 patients with the syndrome of inappropriate antidiuretic hormone secretion to assess the relation of plasma vasopressin to blood pressure in states of acute and chronic vasopressin excess. In the patients with malignant hypertension, vasopressin levels were elevated (13 +/- 2 pg per milliliter. [+/- S.E.M.]) but did not correlate with arterial pressure; however, in normal volunteers, blood pressure did not rise when vasopressin was increased beyond these levels through infusion of the peptide. In the patients with inappropriate antidiuretic hormone secretion, blood pressure was not elevated, but vasopressin was raised (39 +/- 7 pg per milliliter) and did not correlate with systolic or diastolic pressure. These data do not support the concept that an acute or chronic excess of vasopressin makes an important contribution to the regulation of blood pressure.

Adult↗

PubMed2006

Quantitative phosphoproteomics of vasopressin-sensitive renal cells: regulation of aquaporin-2 phosphorylation at two sites.

Protein phosphorylation plays a key role in vasopressin signaling in the renal-collecting duct. Large-scale identification and quantification of phosphorylation events triggered by vasopressin is desirable to gain a comprehensive systems-level understanding of this process. We carried out phosphoproteomic analysis of rat inner medullary collecting duct cells by using a combination of phosphopeptide enrichment by immobilized metal affinity chromatography and phosphorylation site identification by liquid chromatography-mass spectrometry(n) neutral loss scanning. A total of 714 phosphorylation sites on 223 unique phosphoproteins were identified from inner medullary collecting duct samples treated short-term with either calyculin A or vasopressin. A number of proteins involved in cytoskeletal reorganization, vesicle trafficking, and transcriptional regulation were identified. Previously unidentified phosphorylation sites were found for membrane proteins essential to collecting duct physiology, including eight sites among aquaporin-2 (AQP2), aquaporin-4, and urea transporter isoforms A1 and A3. Through label-free quantification of phosphopeptides, we identified a number of proteins that significantly changed phosphorylation state in response to short-term vasopressin treatment: AQP2, Bclaf1, LRRC47, Rgl3, and SAFB2. In the presence of vasopressin, AQP2 monophosphorylated at S256 and diphosphorylated AQP2 (pS256/261) increased in abundance, whereas AQP2 monophosphorylated at S261 decreased, raising the possibility that both sites are involved in vasopressin-dependent AQP2 trafficking. This study reveals the practicality of liquid chromatography-mass spectrometry(n) neutral loss scanning for large-scale identification and quantification of protein phosphorylation in the analysis of cell signaling in a native mammalian system.

Amino Acid Sequence↗

PubMed1974

Conformational studies on arginine vasopressin and arginine vasotocin by proton magnetic resonance spectroscopy.

The assignments and partial conformational analysis of the 220-MHz (1)H nuclear magnetic resonance spectrum of the neurohypophyseal hormones arginine vasopressin and arginine vasotocin in uniformaly deuterated dimethylsulfoxide are reported. The chemical shifts, vicinal coupling constants, temperature coefficients of chemical shifts, and proton-deuterium exchange rates for protons of arginine vasopressin and arginine vasotocin are compared with those for the corresponding protons of the related neurohypophyseal hormones lysine vasopressin and oxytocin. Although to a first approximation the backbone conformations of the hormones exhibit conformational similarities, spectral differences are seen for protons in the amino acid residues that comprise the 20-membered ring moieties. It is inferred that there is a gradual shift in the average conformation in going from arginine vasopressin and lysine vasopressin via arginine vasotocin to oxytocin. As judged on the basis of earlier studies, it is evident that the C-terminal acyclic tail moiety exhibits an enhanced mobility over that of the ring moiety in all of the neurohypophyseal hormones studied and, moreover, that this motion is greater in arginine vasopressin and arginine vasotocin than in oxytocin.

Arginine↗

PubMed1980

Immunological identification of high molecular weight forms common to bovine neurophysin and vasopressin.

Extracts of bovine neurohypophysis made in acid/ethanol solution containing protease inhibitors were fractionated by two successive filtrations on Sephadex G-75 columns equilibrated in the presence and then in the absence of 4 M urea. Analysis of the pattern of neurophysin-like immunoreactivity in the eluate, with two different antibodies, indicated the presence of high M(r) forms of neurophysin (apparent sizes, [unk]70,000 and 20,000-25,000, respectively) besides the M(r) 10,000 neurophysin. [8-Arginine]vasopressin-like immunoreactivity was also detected, coeluting with the neurophysin-like species, in the material recovered in the exclusion and M(r) 20,000-25,000 elution volumes of the same molecular sieve fractionation of neurohypophyseal extracts. Upon subsequent Sephadex G-150 filtration, the immunoreactive material recovered in the exclusion volume of the Sephadex G-75 filtration showed an apparent M(r) of approximately 140,000. Both neurophysin-like and vasopressin-like immunoreactivities coeluted in the same volume. The elution profile of this M(r) 140,000 material was unmodified when reanalyzed by the same molecular sieve filtration after exposure to 8 M urea. When these M(r) 140,000 immunoreactive forms of vasopressin and neurophysin were submitted to affinity chromatography on anti-neurophysin antibodies immobilized on Sepharose, both immunoreactivities were selectively coadsorbed to the immunoadsorbent. Similarly, the neurophysin and vasopressin immunoreactivities associated with M(r) approximately 25,000 were retained together on the same anti-neurophysin immunoadsorbent. The M(r) 140,000 and M(r) 25,000 species having both neurophysin and [8-arginine]vasopressin antigenic determinants generated the two neurosecretory components when exposed to proteolytic activities. This in vitro processing was inhibited in acid medium, at low temperature, and in the presence of a mixture of protease inhibitors. It is concluded that these two large forms of proteins containing both neurophysin and vasopressin may represent common biosynthetic precursors of these two neurohypophyseal components.

Animals↗

PubMed1984

Vasopressin gene is expressed at low levels in the hypothalamus of the Brattleboro rat.

The Brattleboro rat carries as a recessive trait the inability to synthesize hypothalamic vasopressin and its related neurophysin but is able to synthesize oxytocin and its neurophysin. Brattleboro rats homozygous for this trait have no immunologically detectable circulating vasopressin and manifest a complete syndrome of diabetes insipidus, which is corrected with vasopressin replacement therapy. Such a defect could be due to absence of the gene encoding vasopressin, the presence of an abnormal gene, or a variety of transcriptional or posttranscriptional abnormalities. We report here that the hypothalamus of the Brattleboro rat contains detectable, although markedly reduced, levels of an mRNA indistinguishable in size with and similar in sequence to authentic vasopressin mRNA. Corresponding levels of oxytocin mRNA were the same in Brattleboro and normal rat hypothalami. These findings indicate that the Brattleboro rat expresses a vasopressin gene, but at a reduced level.

Amino Acid Sequence↗

PubMed1987

Cell specificity of vasopressin binding in renal collecting duct: computer-enhanced imaging of a fluorescent hormone analog.

A noninvasive microscopic method was used to assess the cell specificity of vasopressin binding within the heterogeneous collecting duct. The binding of a fluorescent vasopressin analog (1-desamino-8-rhodamine-L-lysine vasopressin) to cells of the microperfused rabbit cortical collecting tubule was visualized and quantitated with image-intensified video microscopy and digital image processing. Binding to the basolateral membranes of a subpopulation of cells could be detected within 1-2 min of addition of the fluorescent analog (10 nM) to the peritubular bath. Binding could be prevented or reversed by the addition of a 10-fold excess of the native hormone, which indicates that the fluorescent analog binds specifically to vasopressin receptors. The time course of binding paralleled and slightly preceded hyperpolarization of the lumen-negative transepithelial voltage, an electrical response that is also elicited by the native hormone. Double-label experiments in which the intercalated cell population was stained with fluorescein-labeled peanut lectin revealed that binding of the vasopressin analog was localized to the remaining cell type, the principal cell. Our results support the following conclusions. First, the principal cell constitutes the primary target cell for vasopressin in the rabbit cortical collecting tubule, although the intercalated cell may possess a limited number of receptors at a density below the detection limit of this optical approach. Second, computer-enhanced video microscopy is a powerful, noninvasive method for assessing the kinetics and spatial pattern of hormone binding.

Animals↗

PubMed1989

Central vasopressin infusion prevents hibernation in the European hamster (Cricetus cricetus).

The amount of immunocytochemically detectable vasopressin in the brain of the European hamster (Cricetus cricetus) shows a seasonal variation; i.e., dense vasopressin immunoreactivity is present in the lateral septum during summer but is absent in autumn and winter [Buijs, R. M., Pévet, P., Masson-Pévet, M., Pool, C. W., De Vries, G. J., Canguilhem, B. & Vivien-Roels, B. (1986) Brain Res. 371, 193-196]. In the winter period the European hamster hibernates. Since vasopressin in the lateral septum is known to be involved in the control of body temperature, we investigated whether infusion of vasopressin in the lateral septum during autumn-winter could influence hypothermic patterns normally seen in hibernating animals. Hamsters whose lateral septum was infused with vasopressin showed almost no periods of hypothermia, whereas hamsters treated with control infusions displayed a normal hibernation pattern. The results indicate that persistence of vasopressin release in the lateral septum of the European hamster during winter can prevent hibernation.

Animals↗

PubMed2003

Palmitoylation of the V2 vasopressin receptor carboxyl tail enhances beta-arrestin recruitment leading to efficient receptor endocytosis and ERK1/2 activation.

A large number of G protein-coupled receptors are palmitoylated on cysteine residues located in their carboxyl tail, but the general role of this post-translational modification remains poorly understood. Here we show that preventing palmitoylation of the V2 vasopressin receptor, by site-directed mutagenesis of cysteines 341 and 342, significantly delayed and decreased both agonist-promoted receptor endocytosis and mitogen-activated protein kinase activation. Pharmacological blockade of receptor endocytosis is without effect on the vasopressin-stimulated mitogen-activated protein kinase activity, excluding the possibility that the reduced kinase activation mediated by the palmitoylation-less mutant could result from altered receptor endocytosis. In contrast, two dominant negative mutants of beta-arrestin which inhibit receptor endocytosis also attenuated vasopressin-stimulated mitogen-activated protein kinase activity, suggesting that the scaffolding protein, beta-arrestin, represents the common link among receptor palmitoylation, endocytosis, and kinase activation. Coimmunoprecipitation and bioluminescence resonance energy transfer experiments confirmed that inhibiting receptor palmitoylation considerably reduced the vasopressin-stimulated recruitment of beta-arrestin to the receptor. Interestingly, the changes in beta-arrestin recruitment kinetics were similar to those observed for vasopressin-stimulated receptor endocytosis and mitogen-activated protein kinase activation. Taken together the results indicate that palmitoylation enhances the recruitment of beta-arrestin to the activated V2 vasopressin receptor thus facilitating processes requiring the scaffolding action of beta-arrestin.

Animals↗

PubMedDate not supplied

The effect of vasopressin on organ blood flow in an endotoxin-induced rabbit shock model.

The effects of vasopressin on the vasculature differ from those of other vasopressors, and its effects on the coronary artery remain debatable. This study was undertaken to examine the effects of vasopressin in a rabbit endotoxin-induced shock model and to compare these effects with those of norepinephrine. Thirty rabbits were divided into four study groups: a normal control group (group I, n = 5), a shock control group (group II, n = 5), a vasopressin group (group III, n = 10), and a norepinephrine group (group IV, n = 10). Shock was induced by intravenously infusing lipopolysaccharide (Escherichia coli O111:B4) in groups II, III, and IV. In groups III and IV, systemic blood pressure was maintained to the level of group I by adjusting vasopressin and norepinephrine doses. Left ventricle, right ventricle, ventricular septum, kidney, liver, spleen, and skeletal muscle blood flows were measured using radioisotope tagged microspheres at baseline and 2 h after initial blood flow measurement. No difference in organ blood flows were observed between groups I and II, and coronary blood flow in the left ventricle, right ventricle, and ventricular septum was similar in all study groups. However, renal blood flow was significantly lower in group IV than in group III (p < .05) and hepatic arterial blood flow was significantly lower in group III than in group IV (p < .05). Thus, effect of vasopressin on organ blood flow is organ dependent. Vasopressin increased renal blood flow and decreased hepatic arterial blood flow in this endotoxin-induced shock model, whereas norepinephrine did not. However, coronary blood flow was not changed by shock status or vasopressor type.

Animals↗

PubMed1980

A cytochemical bioassay for arginine vasopressin: preliminary studies.

A new method of measuring vasopressin activity is described. It depends on the finding that the Na+-K+-ATPase activity, measured cytochemically, in the thick ascending limb of the loop of Henle in rat renal tissue maintained in vitro, responded to increasing concentrations of synthetic arginine vasopressin in a log-dose related fashion. The limit of sensitivity was 0.002 pg/ml (2 x 10(-15) mol/l). The dose-responses were reproducible; the inter-assay coefficient of variation was 6.4% at a vasopressin concentration of 0.02 pg/ml. Normal plasma stimulated this Na+-K+-ATPase activity, the stimulation being reduced by 98% when the plasma had been treated with an antiserum specific for vasopressin. Measured in this system, the circulating levels of plasma vasopressin, in healthy adults after 18h dehydration, was 4.0 +/- 0.3 pg/ml (mean +/- SEM; n = 4) and fell to 0.6 +/- 0.1 pg/ml following a water load. Absolute plasma vasopressin values obtained by the cytochemical bioassay were comparable to those measured by radioimmunoassay (r = +0.97, p less than 0.001).

Adenosine Triphosphatases↗

PubMed1989

Very high water permeability in vasopressin-induced endocytic vesicles from toad urinary bladder.

The regulation of transepithelial water permeability in toad urinary bladder is believed to involve a cycling of endocytic vesicles containing water transporters between an intracellular compartment and the cell luminal membrane. Endocytic vesicles arising from luminal membrane were labeled selectively in the intact toad bladder with the impermeant fluid-phase markers 6-carboxyfluorescein (6CF) or fluorescein-dextran. A microsomal preparation containing labeled endocytic vesicles was prepared by cell scraping, homogenization, and differential centrifugation. Osmotic water permeability was measured by a stopped-flow fluorescence technique in which microsomes containing 50 mM mannitol, 5 mM K phosphate, pH 8.5 were subject to a 60-mM inwardly directed gradient of sucrose; the time course of endosome volume, representing osmotic water transport, was inferred from the time course of fluorescence self-quenching. Endocytic vesicles were prepared from toad bladders with hypoosmotic lumen solution treated with (group A) or without (group B) serosal vasopressin at 23 degrees C, and bladders in which endocytosis was inhibited by treatment with vasopressin at 0-2 degrees C (group C), or with vasopressin plus sodium azide at 23 degrees C (group D). Stopped-flow results in all four groups showed a slow rate of 6CF fluorescence decrease (time constants 1.0-1.7 s for exponential fit) indicating a component of nonendocytic 6CF entrapment into sealed vesicles. However, in vesicles from group A only, there was a very rapid 6CF fluorescence decrease (time constant 9.6 +/- 0.2 ms, SEM, 18 separate preparations) with an osmotic water permeability coefficient (Pf) of greater than 0.1 cm/s (18 degrees C) and activation energy of 3.9 +/- 0.8 kcal/mol (16 kJ/mol). Pf was inhibited reversibly by greater than 60% by 1 mM HgCl2. The rapid fluorescence decrease was absent in vesicles in groups B, C, and D. These results demonstrate the presence of functional water transporters in vasopressin-induced endocytic vesicles from toad bladder, supporting the hypothesis that water channels are cycled to and from the luminal membrane and providing a functional marker for the vasopressin-sensitive water channel. The calculated Pf in the vasopressin-induced endocytic vesicles is the highest Pf reported for any biological or artificial membrane.

Animals↗

PubMed1988

Role of vasopressin in experimental heart failure.

Neurohumoral vasoconstrictor systems are activated in heart failure and influence left ventricular function by modifying pre- and afterload. The renin-angiotensin system, sympathetic nerve activity and vasopressin have all been implicated as mechanisms of vasoconstriction. We investigated the vasoconstrictive action of vasopressin by blocking its vascular receptors by a specific antagonist in animal models of heart failure due to rapid right ventricular pacing in dogs and to aortocaval fistula, pulmonary stenosis and aortic stenosis in rats. In all animal models studied, we observed an inappropirately elevated secretion of vasopressin in association with a decreased plasma osmolality. We found only a small reduction of aortic pressure and peripheral vascular resistance following the vasopressin inhibitor. The renin-angiotensin system and sympathetic nerve activity were activated in all animal models. We injected teprotide in order to test the role of angiotensin in the regulation of peripheral vascular tone, and found a much greater decrease of blood pressure and peripheral vascular resistance than caused by the vasopressin antagonist. These experiments suggest that vasopressin and the renin system increase peripheral vascular tone in certain models of heart failure, and demonstrate a much greater importance for the renin system.

Animals↗

PubMed1983

Plasma renin, catecholamine, and vasopressin during nitroprusside-induced hypotension in ewes.

The effect of acute nitroprusside-induced hypotension on plasma renin activity, catecholamine, and vasopressin concentrations was examined in eight chronically catheterized, conscious ewes. Nitroprusside was infused intravenously for one hour at rates adjusted to achieve a 20% decrease in mean blood pressure (dose range: 14-50 mg, or about 5.8-18.5 micrograms X kg-1 X min-1). During hypotension, renin activity increased from 1.39 +/- 0.49 to 3.92 +/- 1.38 ng X ml-1. h-1, catecholamine concentrations remained unchanged, and vasopressin increased from 1.7 +/- 0.4 to 110 +/- 52.7 pg/ml. A significant positive correlation was obtained between total nitroprusside dose and peak vasopressin level (r = 0.749, P = 0.015). No significant change in arterial-blood pH, PO2, PCO2, plasma osmolality, or sodium concentration were observed throughout the experiment, thus eliminating the possibility of osmolar or hypoxic stimuli for the increased renin activity and vasopressin release. The magnitude of vasopressin release found in our studies implies that it plays a more important role than renin in defense against acute hypotension. In addition, the authors experiments suggest that variation in vasopressin release may be responsible for the variation of the dose of nitroprusside required to maintain hypotension.

Animals↗