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)

It is now clear that various hormones and agonists can stimulate the production of lipid mediators from non-phosphoinositide phospholipids. We have investigated the production of diacylglycerol from nonphosphoinositide sources, and we demonstrated that vasopressin and other vasoactive agents stimulate hydrolysis of phosphatidylcholine in a variety of cultured vascular smooth muscle cells of rat and human origin. We used vasopressin to characterize this response and found that vasopressin stimulates phospholipase D activity against phosphatidylcholine in A-10 vascular smooth muscle cells. The vasopressin-stimulated phosphatidylcholine hydrolysis is both time- and concentration-dependent. The half-maximal dose of vasopressin required for phosphatidylcholine hydrolysis (ED50 approximately 1 nM) correlates well with vasopressin binding to A-10 cells (Kd approximately 2 nM). The phosphatidylcholine in A-10 cells can be preferentially radiolabeled with [3H]myristic acid; subsequent treatment with vasopressin stimulates a rapid increase in 3H-labeled phosphatidate (approximately 4 X control values at 3 min), and after a short lag, 3H-labeled diacylglycerol rises and reaches maximal levels at 10 min (approximately 2 X control values). Similar temporal elevations of phosphatidate and diacylglycerol occur in A-10 cells labeled with [3H] glycerol. In A-10 cells radiolabeled with [3H] choline, the elevation of cellular phosphatidate and diacylglycerol is concomitant with the release of [3H] choline metabolites (predominantly choline) to the culture medium. The temporal production of phosphatidate and diacylglycerol as well as the release of choline to the culture medium are consistent with vasopressin activating phospholipase D. In addition, vasopressin stimulates a transphosphatidylation reaction that is characteristic of phospholipase D. The transphosphatidylation reaction is detected by the production of phosphatidylethanol that occurs when A-10 cells are incubated with ethanol and stimulated with vasopressin. The phospholipase D is active in the absence of extracellular Ca++ whereas the vasopressin-stimulated mobilization of arachidonic acid is dependent on extracellular Ca++. The data indicate that vasopressin stimulates phospholipase D which hydrolyzes phosphatidylcholine to phosphatidate. The phosphatidate is then metabolized, presumably by a phosphatidate phosphohydrolase, to produce sustained levels of cellular diacylglycerol. These sustained levels of diacylglycerol may activate protein kinase C and thereby function in the "sustained phase" of cellular responses.
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PMID:Vasopressin stimulates phospholipase D activity against phosphatidylcholine in vascular smooth muscle cells. 228 Jun 71

The maturity of the hypothalamic-neurohypophyseal system in the first 10 days of the postnatal life of rats was analysed through the potential inhibitory effect of ethanol on oxytocin and vasopressin secretion. Experimental animals were intraperitoneally injected with ethanol, and the control ones with the corresponding amount of physiological solution. Hypophyses were extracted 30 min later to be histologically analysed. Although the morphological features of neurohypophysis with functionally active pituicytes and dense vascular net were present even from the first natal day, neurosecretory grains were noticed not before the 8 th day. But the inhibitory effect of ethanol on neurosecretion did not manifest itself until the 10 th day, so it can be concluded that in this period the hypothalamic-neurohypophyseal system had not yet reached its level of complete maturity. Fatty acids in pituicytes being elements of neurohypophyseal neuroglia are pronunced even in animals younger than 10 days, which indicates that their origin could not be necessarily linked to the process of neurosecretion. In acutely alcoholized offsprings the amount of fatty acids in the neurohypophysis was reduced. This is substantiated by the engagement of the alcohol dehydrogenase (ADH) and the microsomal ethanol-oxidizing system (MEOS) in alcohol metabolism with which follows retarded oxidation process of fatty acids.
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PMID:[Reactive characteristics of the neurohypophysis in the early postnatal period]. 228 3

1. In water-loaded rats under ethanol anaesthesia, the injection of 2-4 microliters 1.54M NaCl solution (hypertonic saline:HS) into a lateral cerebral ventricle (i.c.v.) produced an antidiuretic and a pressor response, together with increased urinary excretion of vasopressin and 'oxytocin-like radioimmunoreactivity' (OLRI). In lactating rats HS also produced a milk-ejection response which was shown to be due to the release of oxytocin. 2. The injection of 20-40 micrograms gamma-aminobutyric acid (GABA) or 40-80 ng muscimol i.c.v. 2 min before HS inhibited the antidiuretic, pressor and milk-ejection responses and reduced the urinary excretion of vasopressin and OLRI. 3. The pressor response to HS was abolished by a ganglion blocking agent but it was not reduced by a vasopressin antagonist. After the antagonist, the antidiuretic response to HS was abolished and the pressor response was accompanied by a diuresis both of which were blocked by muscimol. 4. The threshold dose of HS for an antidiuretic response was 4-8 times higher on injection into the cisterna magna (i.cist.) than when injected i.c.v. GABA, i.v. or i.cist, did not inhibit the response to HS i.c.v. 5. The results confirm other evidence that, in the rat, in contrast some other species, an osmotic stimulus causes release of both vasopressin and oxytocin. This release is blocked by GABA and muscimol. These drugs and HS act at a site reached not from the subarachnoid space but from the cerebral ventricles, probably the hypothalamus. The pressor response to HS under the experimental conditions used is due entirely to central sympathetic stimulation and this effect, as well as the release of vasopressin and oxytocin, is blocked by muscimol.
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PMID:Central inhibition by gamma-aminobutyric acid and muscimol of the release of vasopressin and oxytocin by an osmotic stimulus in the rat. 233 82

Central tolerance to the effects of ethanol in rats can be prolonged beyond its normal time of disappearance by administration of vasopressin (AVP) or desglycinamide-arginine-vasopressin (DGAVP) after ethanol withdrawal. While the mechanism underlying this effect is unknown, we have reported that specific depletion of hippocampal serotonin (5-HT) prevents the prolongation of tolerance by DGAVP. The present study explored possible presynaptic interactions between DGAVP and 5-HT terminals in the hippocampus, in relation to tolerance retention. When administered acutely, DGAVP had no effect on the rates of hippocampal or septal 5-HT synthesis in naive rats, as assessed by the NSD 1015 method. Moreover, chronic DGAVP treatment that maintained tolerance did not change the in vivo rate of 5-HT synthesis in the hippocampus or septum. Similarly, no significant differences were found in the levels of hippocampal 5-HT or 5-HIAA. Septal 5-HIAA levels were slightly but significantly lower in ethanol-DGAVP than in ethanol-saline rats. In vitro studies revealed, on the other hand, that addition of AVP to the incubation medium failed to affect the spontaneous and stimulated release of endogenous 5-HT from hippocampal slices. While the lack of changes in hippocampal 5-HT synthesis argues against a presynaptic DGAVP-5-HT interaction, the possibility remains of a peptide modulation of 5-HT postsynaptic actions.
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PMID:Vasopressin-like peptides retain ethanol tolerance in the absence of changes in serotonin synthesis in limbic structures. 243 18

A sensitive, specific and reproducible radioimmunoassay was developed for the measurement of alpha-melanocyte-stimulating hormone (alpha-MSH) in the blood plasma of rat. The assay method is based on a sensitive antiserum raised against alpha-MSH in rabbit. The serum is highly specific to alpha-MSH; a HPLC study of an extract of rat plasma showed that the immunoreactivity was given by alpha-MSH. The basal level of alpha-MSH, measured after a simple extraction with ethanol, was found to be 168.3 +/- 16.3 pg/ml (mean +/- SEM). Ether and lysine-vasopressin appeared to be potent stimuli for the peripheral release of alpha-MSH.
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PMID:Specific radioimmunoassay of alpha-melanocyte-stimulating hormone in rat plasma. 254 36

Nineteen patients were studied during the first 4 days after withdrawal from alcohol. Plasma vasopressin was raised (P less than 0.05) and fluid retention occurred (P less than 0.05), with falls in haematocrit (P less than 0.01) and calculated plasma osmolality (P less than 0.02), which were consistent with expansion of plasma volume. Despite these changes mean total body water was within normal limits although there were substantial inter-individual variations. There was no correlation between any measure of fluid balance and the severity of withdrawal symptoms.
Drug Alcohol Depend 1989 Dec
PMID:Fluid balance, vasopressin and withdrawal symptoms during detoxification from alcohol. 260 99

The effects of intracerebroventricularly (icv.) administered oxytocin (OXT) and lysine-8-vasopressin (LVP) on the development of hypothermic tolerance to ethanol were investigated. Mice equipped with an icv cannula were pretreated with graded doses of OXT or LVP (3 ng, 300 pg, 30 pg or 3 pg/animal) before the daily intraperitoneal ethanol (4 g/kg) injection. Two doses of OXT or LVP (3 ng or 300 pg/animal) blocked the development of hypothermic tolerance to ethanol. Smaller doses of the peptides were ineffective in inhibiting the gradual decrease in hypothermia upon repeated ethanol administration, which effect was observed in the control group. The data presented show that the central administration of these neurohypophyseal peptides blocks the development of tolerance to ethanol.
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PMID:Intraventricular administration of neurohypophyseal hormones interferes with the development of tolerance to ethanol. 271 43

Studies involving fluid homeostasis were carried out in adult Long-Evans rats born to mothers given liquid diets containing 35% of the calories derived from ethanol and compared to offspring of dams given isocaloric liquid diets containing no ethanol. Plasma levels of arginine vasopressin (AVP), plasma and urine osmolality, and urine production were determined in water-sated and water-deprived offspring. In the water-sated condition, the group exposed to alcohol prenatally had plasma levels of AVP seven-fold above control levels. This increase was associated with a large increase in within-group variability. Water consumption was also significantly elevated in the group of fetal alcohol exposed (FAE) rats. Plasma and urine osmolality and urine production were similar to control levels. In the control animals, 24-hr of water deprivation produced the expected increase in AVP, in plasma and urine osmolality, and decrease in urine production. The FAE animals, however, showed parallel changes in plasma and urine osmolality and urine production with no significant change in AVP. Examination of basal glucose metabolic rates in the cerebral structures involved in fluid homeostasis revealed that despite the large increase in AVP levels in the FAE rats, only the neurohypophysis and supraoptic nuclei showed significant increases in activity. These data suggest that fetal alcohol exposure causes a long-term disruption in the central mechanisms regulating vasopressin release and fluid homeostatic responses.
Alcohol
PMID:Arginine vasopressin and body fluid homeostasis in the fetal alcohol exposed rat. 273 78

Microinjection of the muscarinic agonist oxotremorine into the hypothalamic supraoptic (SON) and paraventricular (PVN) nuclei which contain cell bodies of vasopressinergic neurons induced potent antidiuretic effects in water-loaded and ethanol-anesthetized rats. The effects included both decreases in urine outflow and increases in urine osmotic pressure. However, no significant changes in various visceral functions other than antidiuresis such as mean blood pressure, heart rate, respiration rate and rectal temperature were observed when oxotremorine was microinjected into the SON. Only a slight change in mean blood pressure (approx. 10 mmHg decrease) was observed by the microinjection into the PVN. Intravenous preinjection of a vasopressin (AVP) V1 V2 antagonist that has one of the most potent V2 (antidiuretic)-antagonist activities, d(CH2)5-D-Tyr(Et)VAVP, inhibited nearly completely the antidiuretic effects induced by the microinjection of oxotremorine. The results demonstrated that oxotremorine stimulated muscarinic receptors in the hypothalamic SON and PVN, released AVP and induced an antidiuretic effect through AVP-receptors in the kidney.
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PMID:Effect of vasopressin antagonist on antidiuresis by oxotremorine microinjected into the hypothalamic supraoptic and paraventricular nuclei in a water-loaded and ethanol-anesthetized rat. 274 38

Functional tolerance to ethanol can be prolonged by administration of the neuropeptide arginine vasopressin (AVP), which acts at specific CNS receptors. AVP receptors in brain (lateral septum) have been shown to be localized, in part, presynaptically, and the mechanism of action of AVP may thus involve modulation of neurotransmitter release. AVP has also been found to increase the levels of mRNA for the cellular proto-oncogene, c-fos, in the septum and hippocampus. This response to AVP, which may be direct or indirect, may underlie the long-term neuroadaptive effects of the peptide. Studies with vasopressin antagonists have indicated a role for endogenous AVP in modulation of ethanol tolerance, and measurement of hypothalamic vasopressin mRNA by Northern blot analysis and in situ hybridization indicates that chronic ethanol ingestion may alter AVP synthesis. Tolerance to the aversive effects of ethanol has been postulated to influence alcohol drinking behavior in some individuals. Elucidation of the mechanism by which AVP affects ethanol tolerance may eventually lead to pharmacological means to modulate tolerance and, consequently, alcohol intake patterns.
Alcohol Alcohol 1989
PMID:Mechanisms of alcohol tolerance. 275 99


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