Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma vasopressin, arterial blood gas tensions, pH, arterial blood pressure, heart rate and respiration were monitored in conscious rats breathing room air or exposed to varying degrees of hypoxia. A similar series of observations was made in a group of anaesthetized rats and in rats treated with alpha- and beta-adrenergic and dopaminergic blocking agents. The effect of two opioid antagonists on the vasopressin response was also noted. Hypoxia produced an increase in circulating vasopressin concentrations in both conscious and anaesthetized rats. In the conscious animals the increase reached statistical significance when the animals were exposed to 12% oxygen in nitrogen, which produced a fall in arterial PaO2 of 44.7 +/- 5.0%. Guanethidine, phentolamine and propranolol all produced a significant fall in the basal concentrations of vasopressin, while guanethidine, phenoxybenzamine and propranolol blocked the increase seen on breathing 12% oxygen in nitrogen. Naloxone and levallorphan also reduced the vasopressin response to hypoxia. Thus it appears that aminergic pathways play a role in the maintenance of circulating concentrations of vasopressin and in the response to hypoxia. Endogenous opioids also appear to be involved in the hypoxic response.
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PMID:Release of vasopressin in response to hypoxia and the effect of aminergic and opioid antagonists. 663 8

Naloxone increases the electrically induced vasopressin release from rat pituitary neurointermediate lobes under appropriate stimulation conditions. In order to examine a possible role of hypophyseal opioid peptides we studied in vitro the effect of opioid peptides and of naloxone on the electrically induced vasopressin release from the rat neurointermediate lobe or isolated neural lobe of the hypophysis. (D-Ala2,D-Leu5)-enkephalin (5 microM), dynorphin-(1-13) (Dyn; 0.2 microM), beta-endorphin (beta-End; 0.02 and 0.2 microM) and also naloxone (1 or 10 microM) increased the evoked vasopressin release from the neurointermediate lobe, but in higher concentrations (2 microM) Dyn or beta-End had no effect. After removal of the intermediate lobe, beta-End 2 microM inhibited, while naloxone 10 microM did not change the evoked vasopressin release from the isolated neural lobe. These results demonstrate that hypophyseal opioid peptides can influence vasopressin release in several ways and suggest that endogenous opioids predominantly provide inhibitory influences which depend on the presence of the intermediate lobe.
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PMID:Naloxone increases vasopressin secretion from the neurointermediate lobe of the hypophysis of the rat: search for the endogenous agonist. 666 31

The renal response to the acute administration of morphine was examined in conscious, chronically catheterized, nonhydrated rats. After control clearance periods, morphine sulfate was injected i.v. at 4 mg/kg followed by an infusion of 2 mg/kg X hr. Morphine caused an increase in urine flow which was variable in magnitude and duration. The initial diuresis was not maintained despite continued morphine administration and replacement of lost fluid. Compared to vehicle treatment morphine also induced marked sodium and chloride retention which was sustained throughout the 2-hr infusion period. There were no changes in blood pressure or heart during the clearance periods, although an initial transient hypotension and bradycardia were observed with morphine injection. There were no changes in glomerular filtration rate which could account for the antinatriuresis. Naloxone pretreatment blocked all of the observed renal responses. The results indicate that morphine exerts its effects on electrolyte excretion by enhancing renal tubular sodium or chloride reabsorption rather than changes in systemic hemodynamics or glomerular filtration rate. In a separate series of experiments, urine osmolality, osmolar clearance and free water clearance were estimated. All rats receiving morphine transiently excreted a hypotonic urine (minimum 183 +/- 23 mOsmol/kg of H2O) with a reduction in osmolar clearance and a sharp increase in free water clearance. These findings are consistent with a temporary inhibition of vasopressin release by morphine.
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PMID:Antinatriuretic effect of acute morphine administration in conscious rats. 671 65

1. The effects of naloxone on blood pressure recovery after either rapid arterial haemorrhage or prolonged venous haemorrhage were studied in rats lacking vasopressin (Brattleboro strain) and in control (Long Evans) rats. 2. To produce similar reductions in blood pressure, less blood had to be taken from the Brattleboro rats than from the Long Evans rats. 3. After rapid arterial haemorrhage in the absence of naloxone, blood pressure recovery was slower in Brattleboro rats than in Long Evans rats. Naloxone did not affect the response to rapid arterial haemorrhage in Long Evans rats, but improved blood pressure recovery in Brattleboro rats; despite this improvement, the Brattleboro rats remained hypotensive at a time when the Long Evans rats were normotensive. These findings suggest that both the absence of vasopressin and a depressor action of beta-endorphins may contribute to the poor ability of Brattleboro rats to cope with rapid haemorrhage. 4. After prolonged venous haemorrhage in the absence of naloxone, there was no difference between the recovery of blood pressure in Brattleboro rats and Long Evans rats. Naloxone improved blood pressure recovery to a similar extent in both strains of rat. These findings suggest that the absence of vasopressin does not impair blood pressure recovery after prolonged haemorrhage.
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PMID:Effects of haemorrhage in rats lacking vasopressin (Brattleboro strain): influence of naloxone. 685 17

The effect of fusaric acid (FA) on the body temperature of age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) was investigated at an ambient temperature of 4 degrees C. During a 7 h period of cold exposure the body temperature decreased by 6.5 degrees C in WKY (p less than 0.01) and by 5.4 degrees C in SR (p less than 0.05) after administration of 100 mg/kg FA, with the effects occurring faster in WKY. At 50 mg/kg the effect was lower. Naloxone completely abolished the temperature effect of FA in both rat strains. The naloxone antagonism may point to an opiate involvement in the thermoregulation after FA. A possible contribution of vasopressin and tetrahydroisoquinoline alkaloids to the maintenance of body temperature is also discussed.
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PMID:Effect of fusaric acid on the body temperature in spontaneously hypertensive and normotensive rats. 688 9

Stereotactic instillation of absolute alcohol into the sella turcica for pituitary destruction was carried out in 29 patients divided into two groups. Seventeen with prostatic carcinoma underwent a total of 19 injections with 94% good to excellent results that persisted throughout the remainder of the patient's life-span. The longest survival was 9 months. Brief relapses did occur, but spontaneous remissions were the rule. A second group of mixed cancers contained 12 patients who received a total of 13 injections. Eleven patients had good to excellent results that persisted in all but 1 patient. The longest survival was 7 months. Hormonal levels and prolactin stimulation tests failed to show any correlation between hormonal changes and pain relief. Naloxone reversal of analgesia did not occur. There was no loss of cognitive function shown on psychological testing. Pathological studies showed destruction of the pituitary gland, which was subtotal in some patients despite good pain relief. All examinations showed that the pituitary stalk was destroyed. Patients who survived longer also showed degeneration of the supraoptic and paraventricular nuclei of the hypothalamus and the median eminence. All but 1 patient with pain relief exhibited a lack of antidiuretic hormone (ADH) production. Interpretation of the data indicates that ADH or its associated neurophysins act as central pain transmitters. The production of these transmitters is decreased or abolished by chemical hypophysectomy through the destruction of hypothalamic nuclei.
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PMID:Treatment of pain of diffuse metastatic cancer by stereotactic chemical hypophysectomy: long term results and observations on mechanism of action. 699 70

Intravenous nicotine was administered to a group of six subjects during the concurrent intravenous infusion of either the opiate antagonist naloxone, or of saline. Nicotine stimulated vasopressin secretion in all subjects. Naloxone infusion increased both the plasma vasopressin response to nicotine and the resulting rise in urine osmolality.
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PMID:Naloxone increases the nicotine-stimulated rise of vasopressin secretion in man. 709 61

In rats, intracerebroventricular (i.v.t.) administration of endogenous opioid peptides inhibited angiotensin II-stimulated increase in plasma vasopressin concentration and drinking behavior. Naloxone and naltrexone were used to evaluate the effect of opiate receptor blockade on angiotensin drinking behavior. Both antagonists reduced the amount of water consumed and number of animals drinking in response to angiotensin II (i.v.t.). The time to onset of drinking was unaffected. Leucine5-enkephalin inhibition of angiotensin-stimulated release of vasopressin was also studied. Changes in plasma vasopressin concentration with time (5, 45, 90, 150 and 300 sec) were measured after a single i.v.t. injection of angiotensin II (50 ng), with and without pretreatment with leucine5-enkephalin (100 microgram i.v.t.). Vasopressin was measured by radioimmunoassay. The onset of vasopressin release occurred 5 to 45 sec after angiotensin, reaching peak response between 45 to 90 sec. Leucine5-enkephalin did not affect the onset but reduced the peak response to angiotensin (P less than .05). Saralasin, i.v.t., abolished angiotensin-stimulated increase in plasma vasopressin concentration and prevented the residual, but significant, increase in plasma vasopressin concentration in angiotensin-treated rats given enkephalin. It is concluded that angiotensin stimulates release of vasopressin by interaction with specific, saralasin-sensitive, receptors; leucine5-enkephalin inhibits angiotensin release of vasopressin; and an endogenously synthesized opiate ligand(s) may affect angiotensin drinking behavior.
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PMID:Opiate regulation of angiotensin-induced drinking and vasopressin release. 722 96

1. An investigation was carried out to determine the effect of intracerebroventricular (I.C.V.) micro-injections of morphine on vasopressin (AVP) release in the urethane-anaesthetized rat. 2. Plasma AVP levels at different time intervals, following I.C.V. injection of 10-150 microgram morphine, were measured by radioimmunoassay. The effect of I.C.V. micro-injections of morphine on urine outflow was also studied in a group of water-loaded rats. 3. The vasopressin response to I.C.V. micro-injections of morphine was both dose- and time-dependent. High dose of 50 and 150 microgram morphine produced short latency stimulation of AVP release, followed by a fall. The low dose of 10 microgram morphine produced only a long latency inhibition. The most consistent response of I.C.V. injection of morphine was an inhibition of release. 4. Both stimulatory and inhibitory effects of morphine on vasopressin release were naloxone reversible and stereospecific. 5. I.C.V. micro-injections of morphine produced a dose-dependent rise in mean arterial blood pressure of short latency. Naloxone (0.5 mg/kg) completely abolished the rise seen with 10 microgram morphine and diminished the rise with 50 microgram. 6. Doses of 10 and 50 microgram morphine injected I.C.V. produced an immediate antidiuresis in water-loaded rats under urethane anaesthesia. 7. The vasopressin response to I.C.V. micro-injections of morphine is independent of the effects on the cardiovascular system and may involve different opiate receptor populations. The results also suggest the possibility that opiate receptors with different affinities for morphine may be responsible for the stimulatory and inhibitory effects of morphine on vasopressin release.
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PMID:The effect of intracerebroventricular injections of morphine on vasopressin release in the rat. 726 75

The role of endogenous opioids in the control of vasopressin secretion was studied using the pure opiate antagonist naloxone. Naloxone both reduced resting levels of vasopressin and inhibited the rise in vasopressin induced by an orthostatic stimulus. These results suggest that endogenous opioids are important as a tonic stimulus to vasopressin release in man.
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PMID:Evidence for endogenous opioid control of vasopressin release in man. 735 35


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