Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VASOPRESSIN”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,045 records · Page 58Linked to original sources
PubMed2004

Systemic and renal macro- and microcirculatory responses to arginine vasopressin in endotoxic rabbits.

OBJECTIVE: Arginine vasopressin is being used increasingly to treat vasodilatory hypotension, although little is known of its effects on regional perfusion. Arginine vasopressin hemodynamic effects in physiology are mainly mediated through the V1a receptor on blood vessels. To investigate this further, we studied the effect of arginine vasopressin on systemic and renal blood flow in anesthetized, ventilated rabbits given either intravenous saline or endotoxin, and the impact of blocking V1a receptors. DESIGN: Prospective, randomized, controlled study. SETTING: Animal research laboratory. SUBJECTS: Male White New Zealand rabbits. INTERVENTIONS: Measurement was made of mean arterial blood pressure, aortic and renal blood flow velocities (pulsed Doppler), and renal cortical and medullary flow (laser Doppler). MEASUREMENTS AND MAIN RESULTS: In a first series of animals, incremental intravenous boluses of arginine vasopressin ranging from 1 to 1000 ng were administered 90 mins postendotoxin or saline. In control rabbits (n = 9), increasing doses of arginine vasopressin elevated mean arterial blood pressure but reduced both aortic and renal blood flow velocity and renal cortical flow (p <.05). In endotoxic animals (n = 6), arginine vasopressin produced a similar increase in mean arterial blood pressure although aortic flow was maintained while renal blood flow velocity increased, mostly in its diastolic component (p <.05). Pretreatment with the V1a receptor antagonist in a second series of animals blunted all the effects observed in both control (n = 5) and endotoxic (n = 6) animals, suggesting that arginine vasopressin acted mainly through V1a subtype in this early phase of sepsis. CONCLUSIONS: Preservation of renal blood flow with arginine vasopressin during endotoxemia, in particular to the cortex, suggests it could be a promising agent for hemodynamic support during septic shock.

Analysis of Variance↗
PubMed2006

Effects of arginine vasopressin during resuscitation from hemorrhagic hypotension after traumatic brain injury.

OBJECTIVE: Two series of experiments were designed to evaluate whether early arginine vasopressin improves acute outcome following resuscitation from traumatic brain injury and severe hemorrhagic hypotension. DESIGN: Prospective randomized, blinded animal study. SETTING: University laboratory. SUBJECTS: Thirty-three swine. INTERVENTIONS: In series 1 (n = 19), after traumatic brain injury with hemorrhage and 12 mins of shock (mean arterial pressure approximately 20 mm Hg), survivors (n = 16) were initially resuscitated with 10 mL/kg crystalloid. After 30 mins, crystalloid and blood with either 0.1 unit x kg(-1) x hr(-1) arginine vasopressin or placebo was titrated to a mean arterial pressure target >or=60 mm Hg. After 90 mins, all received mannitol and the target was cerebral perfusion pressure >or=60 mm Hg. To test cerebrovascular function, 7.5% inhaled CO2 was administered periodically. In series 2 (n = 14), the identical protocol was followed except the shock period was 20 mins and survivors (n = 10) received a bolus of either arginine vasopressin (0.2 units/kg) or placebo during the initial fluid resuscitation. MEASUREMENTS AND MAIN RESULTS: In series 1, by 300 mins after traumatic brain injury with arginine vasopressin (n = 8) vs. placebo (n = 8), the fluid and transfusion requirements were reduced (both p < .01), intracranial pressure was improved (11 +/- 1 vs. 23 +/- 2 mmHg; p < .0001), and the CO2-evoked intracranial pressure elevation was reduced (7 +/- 2 vs. 26 +/- 3 mm Hg, p < .001), suggesting improved compliance. In series 2, with arginine vasopressin vs. placebo, cerebral perfusion pressure was more rapidly corrected (p < .05). With arginine vasopressin, five of five animals survived 300 mins, whereas three of five placebo animals died. The survival time with placebo was 54 +/- 4 mins (p < .05 vs. arginine vasopressin). CONCLUSIONS: Early supplemental arginine vasopressin rapidly corrected cerebral perfusion pressure, improved cerebrovascular compliance, and prevented circulatory collapse during fluid resuscitation of hemorrhagic shock after traumatic brain injury.

Animals↗
PubMed2004

Subcellular vasopressin mRNA trafficking and local translation in dendrites.

Vasopressin mRNA is delivered to axons and dendrites of rat hypothalamic magnocellular neurones. Subcellular localization of mRNAs requires sequences (cis-acting elements) within the RNA and proteins (trans-acting factors), which together mediate nucleic acid transport along the cytoskeleton to specific cytoplasmic destinations. In cultured neurones, vasopressin mRNA transcribed from a microinjected eukaryotic expression vector is sorted to dendrites. Detailed analyses revealed the presence of a complex cis-acting element, called dendritic localizer sequence (DLS), within part of the coding- and the 3'-untranslated region of vasopressin mRNA. Biochemical investigations have shown a specific interaction of poly(A)-binding protein (PABP) with the DLS. PABP is implicated in translation, translational control, RNA stability and RNA transport. Hence, PABP could be a component of a probably multifactor complex regulating transport and local translation of vasopressin mRNA. Dendrites are capable of translation. Local synthesis of the vasopressin precursor in dendrites of in vitro cultured neurones was demonstrated by microinjecting a vector encoding a mutant vasopressin polyprotein that is unable to leave the rough endoplasmic reticulum. Expression of this construct revealed that the nondiffusable protein is only detectable in dendrites harbouring vasopressin mRNA whereas dendrites devoid of this transcript lack the mutant vasopressin precursor.

Animals↗
PubMed1993

Effects of novelty stress on vasopressin and oxytocin secretion by the pituitary in the rat.

Effects of novel environmental stimuli on vasopressin and oxytocin secretion by the pituitary were studied in dehydrated male rats. As the novel environmental stimuli, rats were transferred to an experimental room, placed in a box painted black and given a pure tone auditory stimulus of 2 kHz. Exposure of rats to the novel environmental stimuli for a period of 2 min decreased plasma concentrations of vasopressin and increased plasma levels of adrenocorticotrophic hormone (ACTH) and prolactin, but did not significantly change the plasma level of oxytocin. The stimuli, however, became ineffective for producing the suppressive vasopressin response as the period of exposure was prolonged to more than 5 and up to 30 min, although the prolonged stimuli were still effective for inducing facilitatory ACTH and prolactin responses. After repeated exposures of rats to the environmental stimuli once a day for 5 or 10 days, the stimuli became disabled from producing the suppressive vasopressin response. However, the rats were still capable of responding to the novel stimuli of another kind. All these data suggest that novelty stress suppresses vasopressin secretion but does not change oxytocin secretion. In order to test the possibility that glucocorticoids expectedly secreted by the adrenals in response to the stress might have suppressed vasopressin secretion, a large amount of dexamethasone was administered to the rat before testing. Dexamethasone pretreatment depressed plasma levels of ACTH and vasopressin as reported previously and blocked the facilitatory ACTH response to the novelty stress. However, dexamethasone treatment did not affect the suppressive vasopressin response to the novelty stress.(ABSTRACT TRUNCATED AT 250 WORDS)

Acoustic Stimulation↗
PubMed1995

Comparison of the number of vasopressin-producing hypothalamic neurons in rats and humans.

The aim of this study was to assess the number and proportion of vasopressin-producing neurons in the hypothalamic magnocellular nuclei in rats and humans. Accurate and unbiased neuronal counts were estimated using the optical disector method. Arginine vasopressin-containing neurons were immunohistochemically visualized in formalin-fixed tissue sections. The magnocellular neurons were similar in size and morphology in both species. While the human hypothalamus contained significantly more vasopressin-containing neurons compared with the rat (36-fold increase), the proportion of vasopressin-containing neurons between species was similar. In both species, the majority of supraoptic neurons contained vasopressin, however the proportion of vasopressin-containing neurons in the human paraventricular nucleus was double that of the rat (nearly a 100-fold increase in number). These results suggest that the paraventricular nucleus contributes significantly to the release of vasopressin from the posterior pituitary in humans, whereas in rats vasopressin is mainly released by supraoptic neurons.

Animals↗
PubMed2003

The Hormone Domain of the Vasopressin Prohormone is Required for the Correct Prohormone Trafficking Through the Secretory Pathway.

It has long been known that under intracellular conditions vasopressin associates tightly to neurophysin, which is present in the same prohormone. As the association has been suggested to play a role during hormone biosynthesis, its role was studied in a cellular context by expressing mutant vasopressin precursors in Neuro2A cells. Mutant vasopressin precursors, in which the association between the vasopressin and neurophysin domains was prevented either by deleting the vasopressin domain from the precursor or by substitution of the essential Tyr2 residue in vasopressin for Gly, were neither processed nor targeted into secretory granules. Rather, both provasopressin mutants were retained in the endoplasmic reticulum. Our results demonstrate that the vasopressin domain is crucial for correct trafficking of the prohormone through the secretory pathway, and suggest that vasopressin-neurophysin association provides correct prohormone folding in the endoplasmic reticulum.

Animals↗
PubMed2006

Efficacy and efficiency of gastric electrical stimulation with short pulses in the treatment of vasopressin-induced emetic responses in dogs.

The aim of this study was to determine the most effective and efficient anti-emetic parameters of short-pulse gastric electrical stimulation (GES) in dogs. Seven female beagle dogs implanted with four pairs of gastric electrodes were studied in eight randomized sessions (saline, vasopressin, and six GES sessions with different parameters). Each session consisted of four 20-min recordings of gastric slow waves and symptoms. In sessions 1 and 2, saline and vasopressin, respectively, were infused during the second 20-min period. The protocol of the other six sessions was the same as session 2 except that GES was continuously applied. It was found that: (1) vasopressin induced gastric dysrhythmia and emetic response (P < 0.01, anova); (2) short-pulse GES with a frequency of 14 or 40 Hz and pulse width of 0.1 or 0.3 ms, but not 0.6 ms was able to reduce symptoms induced by vasopressin; (3) short-pulse GES with a pulse width of 0.3 ms was the most effective in preventing vasopressin-induced symptoms; (4) none of the tested GES methods improved vasopressin-induced gastric dysrhythmia. We conclude that vasopressin induces gastric dysrhythmia and symptoms. Short-pulse GES with a pulse width of 0.3 ms and frequency of 14 Hz is most effective and efficient in preventing vasopressin-induced emetic responses in dogs.

Animals↗
PubMed2000

Behavioural impact of intraseptally released vasopressin and oxytocin in rats.

The two nonapeptides arginine vasopressin and oxytocin are not only secreted from the neurohypophysis into the general circulation but are also released intracerebrally. Our recent research has focused on the release patterns and effects of oxytocin and vasopressin in brain areas, such as the septum and hypothalamus, that are thought to be involved in the regulation of (1) behavioural responses and (2) responses of the hypothalamo-neurohypophysial system (HNS) to stressor exposure in rats. The results demonstrate that combined physical and emotional stress (induced by exposure to forced swimming) selectively triggers the release of vasopressin within all brain areas under study but not into the general circulation. Under emotional stress conditions (induced by exposure to the 'social defeat' procedure), however, oxytocin rather than vasopressin release increased within the hypothalamus and septum. Experiments aimed at revealing the neuroendocrine and behavioural relevance of the local nonapeptide release provided evidence for an involvement of vasopressin in the regulation of HNS activity (within the hypothalamus) and, moreover, in acute stress-coping strategies, anxiety-related behaviour and learning and memory processes (within the septum). The observed dissociation between central and peripheral nonapeptide release not only supports the hypothesis that plasma vasopressin and oxytocin concentrations do not necessarily reflect central release patterns but also suggests vasopressin and oxytocin neurones are able to independently release their nonapeptide from different parts of their neuronal surface (e.g. from somata/dendrites vs. axon terminals). This remarkable regulatory capacity provides the basis for an differential involvement of vasopressin, and probably also oxytocin, in the co-ordination of neuroendocrine activity, emotionality and cognition at different brain levels to ensure an appropriate behavioural response of the organism to stressful stimuli.

Animals↗
PubMed2000

Control of the renal medullary circulation by vasopressin V1 and V2 receptors in the rat.

Utilization of the acute and chronically instrumented Sprague-Dawley rat model has provided new and informative data about the mechanisms of, and the role that circulating arginine vasopressin plays in, the regulation of blood flow to the renal medulla. Regional changes of blood flow were measured using implanted optical fibres and laser-Doppler flowmetry techniques. Transcriptional and translational sites of the V1a and V2 receptors were determined in microdissected intrarenal vascular segments from the cortex and medulla. Results from acute and chronic studies indicate the following. First, physiological elevations of plasma vasopressin concentration seen with 48 h of water restriction reduce blood flow to the inner medulla (via V1 receptors) while maintaining a constancy of blood flow to the outer medulla. Reduction of medullary blood flow is necessary to optimize urine osmolality during water restriction. Second, increases of plasma vasopressin concentration of as little as 8 pg ml(-1), which produce no change in baseline arterial pressure or renal cortical blood flow, can lower medullary blood flow selectively and greatly attenuate the arterial pressure-blood flow and pressure-natriuresis relationship. Third, medullary blood flow does not remain reduced in the face of sustained elevations of plasma vasopressin concentration, which appears to be related to the inability of vasopressin to produce a sustained hypertension. Fourth, V1a receptor mRNA and protein are present in the isolated cortical and medullary vasculature, but the V2 receptor mRNA and protein are found only in tubular segments. Levels of V2 receptor mRNA during water restriction were quantified using a competitive RT-PCR and a deletion mutant RNA transcript to control for the efficiency of the reaction, and Western blot analysis was utilized for quantification of the V2 receptor protein. The results demonstrated a time-dependent downregulation of the V2 receptor mRNA and protein within the rat kidney, specifically in the outer medulla. Fifth, the vasopressin-induced vasoconstriction of the medullary vasa recta microvessels was shown to be mediated via V1a receptors, and this response is normally modulated by vasopressin-stimulated release of nitric oxide (NO), via extravascular (presumably medullary collecting duct ) stimulation of V2 receptors. Finally, chronic vasopressin administration (10 days) increased nitric oxide synthase activity in the outer medulla and interstitial NO concentration in the medulla. These changes are essential to provide a constancy of blood flow to the renal medulla and buffer against the hypertensive actions of this potent vasoconstrictor peptide.

Animals↗
PubMed1994

Intramyometrial vasopressin as a haemostatic agent during myomectomy.

OBJECTIVE: To assess the efficacy of intramyometrial vasopressin for minimising bleeding and its sequelae at myomectomy. DESIGN: A randomised placebo controlled trial. SETTING: University Hospital of the West Indies, Kingston, Jamaica. SUBJECTS: Twenty women with symptomatic uterine fibroids scheduled for myomectomy who satisfied entry criteria: 10 randomised to the vasopressin group and 10 to the control group. INTERVENTION: Myomectomy was performed after the intramyometrial injection of either 20 units vasopressin diluted to 20 ml in normal saline or placebo (20 ml normal saline). MAIN OUTCOME MEASURES: The efficacy of vasopressin was measured by comparing pre- and post-operative haemoglobin levels and haematocrit, changes in intra-operative pulse and blood pressure, measured blood loss, need for blood transfusion and post-operative febrile morbidity in the treatment and control groups. RESULTS: The use of vasopressin resulted in median blood loss of 225 ml (range 150-400 ml) compared with 675 ml (range 500-800 ml) in the placebo group (P < 0.001). The vasopressin group had a correspondingly lower fall in haemoglobin level (median 1.7 g/dl vs 5.3 g/dl, P < 0.001) and haematocrit (median 5% vs 13%, P < 0.001) compared with the controls. Fifty percent of the placebo group had blood transfusions compared with none in the vasopressin group (P = 0.03). There were no significant differences between the groups in intra-operative pulse and blood pressure or post-operative white blood cell counts or temperature. CONCLUSION: The results indicate that vasopressin is effective in preventing blood loss and reducing the need for blood transfusion during myomectomy.

Adult↗
PubMed1978

Vasopressin release produced in anaesthetized cats by antagonists of gamma-aminobutyric acid and glycine.

1 In cats anaesthetized with chloralose, the central excitatory substances, tubocurarine, picrotoxin, bicuculline, leptazol and strychnine, were applied to the exposed ventral surface of the brain stem through paired Perspex rings placed across the medulla and their effects on vasopressin release and arterial blood pressure were examined.2 The excitatory substances released large amounts of vasopressin when applied to an area 6-9 mm caudal to the trapezoid bodies. From this area vasopressin release was previously obtained with nicotine.3 With nicotine, the vasopressin release occurred almost instantaneously and tachyphylaxis developed rapidly. With the excitatory substances the release increased gradually and there was no tachyphylaxis. When these substances were applied for several minutes, the release reached its maximum a considerable time after their removal, except with leptazol when release diminished at once after removal.4 The excitatory substances had little or no effect on arterial blood pressure when applied to the vasopressin releasing area, but produced strong pressor responses when applied to a more rostrally situated area.5 It is concluded that the excitatory substances release vasopressin and raise arterial blood pressure because they are antagonists of gamma-aminobutyric acid and/or glycine and that numerous inhibitory neurones which release these amino-acids synapse at the ventral surface of the medulla. The physiological function of those which synapse at the vasopressin releasing area may be to act as a brake on vasopressin release, and of those which synapse at the more rostrally situated area to act as a brake on arterial blood pressure.

Aminobutyrates↗
PubMed1990

Vasopressin and stress-induced antinociception in the mouse.

1. Arginine vasopressin produced antinociception in the hot-plate test after intracerebroventricular injection (0.5 micrograms) and in the acetic acid abdominal constriction test after intraperitoneal injection (0.1 mg kg-1). 2. The antinociception produced by arginine vasopressin was sensitive to deamino(CH2)5Tyr(Me) arginine vasopressin (0.5 micrograms i.c.v.; 0.1 mg kg-1 i.p.) but not to naloxone (5 micrograms i.c.v.; 2 mg kg-1 i.p.) 3. Arginine vasopressin when administered by the intracerebroventricular route, but not by the intraperitoneal route, produced characteristic behaviour which was sensitive to deamino(CH2)5Tyr(Me) arginine vasopressin (0.5 micrograms, i.c.v.). 4. A 3 min swim at 20 degrees C produced antinociception on the hot-plate which was sensitive to naloxone (0.4 mg kg-1, i.p.) but not to deamino(CH2)5Tyr(Me) arginine vasopressin (0.5 micrograms, i.c.v.). 5. The reduction in the number of acetic acid-induced abdominal constrictions produced by a 30 s swim at 30 degrees C was not sensitive to either naloxone (2 mg kg-1, i.p.) or deamino(CH2)5Tyr(Me) arginine vasopressin (0.1 mg kg-1, i.p.). 6. Arginine vasopressin, at high doses, is antinociceptive in the mouse but does not appear to mediate stress-induced antinociception in this species.

Animals↗
PubMed1997

Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation.

OBJECTIVES: To determine the hemodynamic effect of vasopressin on coronary perfusion pressure (CPP) in prolonged human cardiac arrest. METHODS: A prospective, open-label clinical trial of vasopressin during cardiac resuscitation was performed. Ten patients presenting in cardiac arrest initially received resuscitative measures by emergency physicians according to Advanced Cardiac Life Support (ACLS) guidelines. A central venous catheter for fluid and drug administration and a femoral artery catheter for measurement of CPP (aortic minus right atrial relaxation phase pressures) were placed. When each patient was deemed nonsalvageable, 1.0 mg epinephrine was given and CPP was measured for 5 minutes, followed by a dose of vasopressin (1.0 U/kg). CPP measurements were continued for another 5 minutes. RESULTS: The mean duration of cardiac arrest (out-of-hospital interval plus duration of ED ACLS) was 39.6 +/- 16.5 min. There was no improvement in CPP after 1.0 mg of epinephrine. Vasopressin administration resulted in a significant increase of CPP in 4 of the 10 patients. Patients responding to vasopressin had a mean increase in CPP of 28.2 +/- 16.4 mm Hg (range: 10-51.5), with these peak increases occurring at 15 seconds to 4 minutes after administration. The increases in the vasopressin levels after administration did not differ between the responders and nonresponders. CONCLUSIONS: In this human model of prolonged cardiac arrest, 40% of the patients receiving vasopressin had a significant increase in CPP. This pilot study suggests that investigation of earlier use of vasopressin as a therapeutic alternative in the treatment of cardiac arrest is warranted.

Adult↗
PubMed1988

Control of release of vasopressin by neuroendocrine reflexes.

The neurones in the supraoptic and paraventricular nuclei (SON and PVN) which secrete vasopressin are separate from those which secrete oxytocin and are distributed in different parts of the nuclei. They may be distinguished electrophysiologically by a characteristic phasic pattern of firing. A selective afferent neural input to these neurones would provide a mechanism for the release of vasopressin independently of oxytocin in response to appropriate physiological stimuli. Release of vasopressin is controlled by changes in blood volume or pressure ('volume control') and in plasma osmolality ('osmotic control'). Stimuli involved in volume control such as haemorrhage, hypotension and carotid occlusion cause vasopressin to be released into the circulation with little or no detectable oxytocin. An osmotic stimulus releases vasopressin alone in some species but not apparently in the rat in which both hormones are released. Volume control is mediated reflexly by peripheral receptors in the cardiovascular system. Activation of baro- and stretch receptors results in inhibition, and activation of chemoreceptors in stimulation, of release. Afferent impulses from these receptors are conveyed in the vagi and carotid sinus nerves to the NTS on the dorsal surface of the brain stem. All afferent impulses to the NTS are excitatory. It follows that the afferents from chemoreceptors must stimulate an excitatory, and those from baro- and stretch receptors an inhibitory, projection from the NTS to the vasopressin-secreting cells in the SON and PVN. Two alternative models are presented of the neural pathways and transmitters involved. The model of Fig. 2 shows an excitatory relay through a cholinoceptive area on the ventral surface of the brain stem which has been termed the 'nicotine-sensitive area' because topical application of nicotine to this area in the cat released vasopressin without oxytocin. An inhibitory relay is shown through the A1 group of noradrenergic neurones on the ventral surface which selectively innervate the vasopressin-secreting neurones in the SON. This model implies an inhibitory role for noradrenaline acting on beta- or alpha 2-receptors. However the most recent investigations suggest an excitatory, rather than inhibitory, function of the A1 noradrenergic neurones involving alpha 1-receptors. This is the basis of the model in Fig. 3. The A1 neurones project either directly to the SON and PVN or indirectly through the lateral preoptic nucleus which lies in close proximity to the SON. The nicotine-sensitive area may be coincident with the A1 group of noradrenergic neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1972

Vasopressin clearance and secretion during haemorrhage in normal dogs and in dogs with experimental diabetes insipidus.

1. The secretion of vasopressin in response to haemorrhagic shock has been investigated in anaesthetized dogs.2. The changes in the plasma concentrations of vasopressin were followed over a period of 5 hr, during which the arterial blood pressure was kept constant at 40 mm Hg. It was found that vasopressin concentration in plasma rose to a high peak shortly after the onset of shock and gradually declined thereafter. Five hours later, it was still 3.5 times higher than control. Re-transfusion of blood was followed by a return to control levels.3. The clearance of vasopressin was calculated before and during shock in normal dogs and in dogs with experimental diabetes insipidus. Soon after the onset of shock, the clearance rate dropped to one quarter of its normal level but slowly recovered, returning to near control values at the fifth hour of shock. Clearance rates did not vary as a function of infusion rates, suggesting that there is no maximal transport rate for the removal of the hormone over the entire secretory range found in normal and hypotensive dogs.4. From the clearance rates and from the plasma concentrations of endogenously secreted vasopressin it has been possible to calculate the approximate secretory rates of the hormone in response to shock. Secretion rose to a very high level, some 40 times greater than control, at the onset of shock. This was followed by a fairly constant secretory plateau. At the fifth hour of shock secretion was 3.5 times higher than control.5. The half-life of vasopressin was measured in normal and hypotensive dogs. Control measurements confirm the generally accepted value of approximately 5 min. The half-life was significantly higher in the early stage of shock, but returned to control values in the later stage.6. Haemorrhage experiments performed in normal and diabetic dogs suggest that vasopressin may play a part in the development of irreversible haemorrhagic shock: all normal animals died within a few hours of retransfusion, whereas four out of eight diabetic dogs similarly treated survived a 24 hr observation period. In a separate set of experiments, eight diabetic dogs were subjected to the haemorrhage procedure while receiving a constant infusion of vasopressin: only two of these survived. Surviving dogs showed none of the characteristic lesions of irreversible haemorrhagic shock.

Animals↗
PubMed1975

Effect of steroid depletion on the response of toad bladder to vasopressin.

1. We have investigated the water transport and short-circuit current (s.c.c.) response to vasopressin (1 mu./ml. and 100 mu./ml.) in isolated toad urinary bladders (Bufo marinus) following overnight incubation in the presence or absence of steroid-containing Ringer solution. 2. The water transport response to the lower dose of vasopressin (1 mu./ml.) was considerably reduced in 'steroid depleted' conditions, wheras the response to the higher dose of vasopressin (100 mu./ml.) was not similarly affected. 3. Aldosterone 3. Aldosterone 3. Aldosterone (10(-7)M) potentiated the water transport response to the lower dose of vasopressin (1 mu./ml.) but had no effect on the response to the higher dose (100 mu./ml.). 4. There was no effect of 'steroid depletion' or aldosterone treatment on the vasopressin s.c.c. response when measured as a percentage increase above basal levels. 5. In 'steroid depleted' conditions vasopressin (1 mu./ml.) maximally stimulated Na+ transport (s.c.c.) but a higher dose of vasopressin (100 mu./ml.) was required for maximum water transport. 6. We have failed to obtain any potentiation effect of corticosterone (10(-7)M) on the water transport or s.c.c. response to vasopressin (1 mu./ml.).

Adrenal Cortex Hormones↗
PubMed1982

Osmotic water flow across the abdominal skin of the toad bufo marinus: effect of vasopressin and isoprenaline.

1. Net water flow J(w), was measured across the abdominal skin of the toad Bufo marinus with a volumetric, automatic technique that allows for averaging J(w) over time intervals as short as 1 sec.2. Basal J(w) was very stable and corresponded to a coefficient of osmotic flow, L(PD), of ca. 15 x 10(-7) cm sec(-1) atm(-1) (or to an osmotic water permeability coefficient, P(f), of 20 mum sec(-1)).3. Both vasopressin and the beta-adrenergic agonist, isoprenaline, triggered high hydrosmotic responses that could lead to P(f) values exceeding 250 mum sec(-1). The effect of isoprenaline was very reproducible while that of vasopressin varied considerably.4. Methohexital and propranolol selectively inhibited the hydrosmotic effects of vasopressin and isoprenaline, respectively, whereas amiloride and ouabain had no effect.5. Mutual inhibition was found between vasopressin and isoprenaline in skins very sensitive to vasopressin. In less sensitive skins isoprenaline further increased J(w) despite exposure of the epithelia to supramaximal concentrations of vasopressin.6. Differential reactivity to vasopressin was found between the skin and the bladder taken from the same toad. In some instances, the bladder responded normally to vasopressin while the skin was totally unresponsive, suggesting the presence of osmoregulatory mechanisms exerting a local modulation of the vasopressin action in different target epithelia of the same animal.

Animals↗
PubMed1983

Influence of vasopressin and calcium on electrolyte transport across isolated colonic mucosa of the rat.

Vasopressin enhanced the absorption of water and Na+ across everted sacs of rat colon descendens but had no effect on absorption across the colon ascendens. The short-circuit current (Isc) and open-circuit potential difference (p.d.) across the colon descendens were dose-dependently decreased by vasopressin. Isc and p.d. across the colon ascendens were not altered by vasopressin. In the colon descendens the decrease in Isc and p.d. was significant at 1 microu. vasopressin/ml and reached a maximum at 1 mu./ml. Propranolol and phentolamine or naloxone did not alter the decrease in Isc and p.d. to a submaximal dose of vasopressin. Vasopressin increased the mucosal to serosal flux of Na+ and Cl- and decreased the serosal to mucosal flux of Cl- across short-circuited colon descendens. Consequently these changes increased the net flux of Na+ and Cl-. Adenylate cyclase activity in homogenates of the colon descendens was not altered by vasopressin. Omission of Ca2+ from the serosal bathing solution reversibly decreased Isc and p.d. and increased Na+ and Cl- absorption across the colon descendens in a similar way as did vasopressin. The results suggest that the effect of vasopressin on the colon descendens may be due to a decrease in intracellular Ca2+ activity.

Adenylyl Cyclases↗