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)

Sheep were depleted of water by restricting water intake to 500 ml/day for 7-9 days and were then rehydrated by three treatments: voluntary intake of water, administration of water by tube into the stomach, or voluntary intake of 0.9% NaCl solution (saline). The volumes of fluids drunk within 2-3 min, or administered by tube, were approximately equal to the animal's weight loss. Plasma vasopressin rose from 4.4 +/- 0.6 to 16.8 +/- 1.0 pg/ml during water restriction. After drinking water plasma vasopressin fell from 19.0 +/- 1.9 to 7.5 +/- 0.4 pg/ml (P less than 0.001) in 15 min and gradually fell to 3.2 +/- 0.4 pg/ml over 6 h. Plasma osmolality fell from 302.4 +/- 0.9 to 301.0 +/- 1.1 mosmol/kg (NS) 15 min after water drinking and then gradually fell to subnormal levels. Sheep given water by stomach tube showed a similar decline in plasma osmolality, but the fall in plasma vasopressin was attenuated. The fall in plasma vasopressin in the first 30 min after drinking saline was almost identical with the fall after drinking water, but plasma osmolality was unaltered. Plasma vasopressin fell so rapidly after drinking water or saline as to suggest that the act of drinking caused almost complete inhibition of vasopressin release without a change in plasma osmolality. The results are consistent with earlier evidence that oropharyngeal receptors initiate the inhibition of vasopressin release after drinking.
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PMID:Acute reduction of plasma vasopressin levels by rehydration in sheep. 391 58

1. When applied directly to the brain, angiotensin II amide, as either the valine(5) octapeptide, causes rats in normal fluid balance to drink water.2. The drinking response to angiotensin injections is copious, rapid, repeatable within the same test session, and stable over months of testing in the same animal.3. The response is motivationally potent and specific. After injection the animals move directly to the source of water and drink. There is typically no preliminary hyperactivity or subsequent depression. The animals do not eat, gnaw or exhibit other behaviours that are not normally seen during spontaneous drinking. The injections rouse sleeping animals to drink and interrupt eating in animals deprived of food for two days.4. The region of the brain that is most sensitive to angiotensin includes the anterior hypothalamus, the preoptic region, and the septum including the nucleus accumbens.5. Intracranial renin elicited drinking. Bradykinin and vasopressin did not, nor did adrenaline, noradrenaline or aldosterone. In the most sensitive region, sites positive for angiotensin also yielded drinking to carbachol.6. Responses were obtained with 5 ng (ca. 5 p-mole) and occurred reliably with 50 ng angiotensin or more. The dose-response curve for amount drunk rose from 5 to 100 ng and levelled off thereafter. Angiotensin is therefore the most potent dipsogen known and is effective at doses that are reasonably within the concentration range for circulating endogenous angiotensin.7. Injections into the sensitive region of doses of angiotensin that were effective for drinking did not produce peripheral haemodynamic changes in lightly anaesthetized rats.8. This work strengthens the suggestion that angiotensin is a natural hormone of drinking behaviour that participates in extracellular thirst by its release from the kidney and subsequent direct action on a specific chemoreceptive region in the anterior diencephalon and limbic lobe.
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PMID:Drinking induced by injection of angiotensin into the rain of the rat. 432 23

Studies were carried out to determine the relationship between daily sodium intake, drinking, and vasopressin (AVP) secretion in normal conscious dogs. Chronic responses to 5-day elevations of daily sodium intake (200 meq/day) and 2-wk decreases in daily sodium intake (5 meq/day) were determined. Dogs were studied with ad libitum drinking and with water intake restricted to the amount drunk during the normal-sodium (30 meq/day) control period. Although acute elevations of plasma AVP occurred after a normal (40 meq Na) gastric load, chronic high-sodium intake resulted in no change of steady-state plasma AVP levels or daily AVP excretion (UAVP) with ad libitum drinking. Total water intake and frequency of drinking, however, increased nearly fourfold. In the absence of excess drinking, plasma AVP and UAVP both exhibited a nearly sixfold increase during the period of high-sodium intake. Despite elevations of plasma AVP, daily urine volume increased and urine osmolality rose only gradually during the 5 days of high-sodium intake. Chronic low-sodium intake also did not alter plasma AVP, but total water intake was reduced 20%. The data indicate that with water available, extracellular osmolality is controlled predominantly by drinking rather than by AVP secretion, that either osmolality or sodium concentration is the predominant controller of drinking and AVP secretion, and that daily water excretion need not be related directly to plasma AVP.
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PMID:Influence of daily sodium intake on vasopressin secretion and drinking in dogs. 636 37

Within the anterior wall of the third cerebral ventricle, structures are found which have been implicated in the regulation of fluid and electrolyte balance. These structures include the subfornical organ (SFO), preoptic medianus nucleus (PMN) and the organum vasculosum of the lamina terminalis (OVLT). In sheep, the OVLT rises from the ventricular floor over the optic chiasma and occupies most of the midline ventricular wall up to the level of anterior commissure. It contains a plexus of blood vessels at its base which possess fenestrated endothelial cells, and appears to lack ependyma. The SFO of sheep bulges into the third ventricle above the anterior commissure and the PMN is situated between the SFO and OVLT, surrounding the rostral edge of the midline anterior commissure. Like most mammals, water deprivation in sheep results in hypertonicity of body fluids, thirst and graded increase in plasma concentration of vasopressin (AVP). Dehydration also causes a natriuresis in these animals. In sheep with combined ablation of OVLT/PMN tissue, the volume of water drunk, the increases in plasma vasopressin (AVP) level, and the natriuresis in response to dehydration were considerably attenuated, and extreme hypernatremia resulted. Additionally, ablation of OVLT/PMN tissue almost abolished water drinking and AVP secretion in response to systemic infusion of hypertonic NaCl, but did not diminish AVP secretion in response to haemorrhage. In other animals, the OVLT and PMN were individually ablated. While partial osmoregulatory deficits were observed in each case, these deficits were smaller than those observed with combined OVLT/PMN ablation. In contrast to these results, the homeostatic responses to dehydration were not diminished in sheep with combined SFO/PMN lesions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The anterior wall of the third cerebral ventricle and homeostatic responses to dehydration. 653 50

The effects of ablation of the nucleus medianus on drinking and vasopressin secretion were studied in male Long-Evans rats. The amount of water drunk in 1 h was assessed after subcutaneous injection of 5.8% NaCl (13.34 mosm/kg) or of angiotensin II (1.5 mg/kg). In a separate test with no water available, plasma vasopressin was measured 15 min after the above dose hypertonic saline. Ablation of the nucleus medianus, or the dorsal and anterior portions of the nucleus medianus, blocked drinking to hypertonic saline or angiotensin II and attenuated the vasopressin response to hyperosmolality. Animals with septal or diagonal band lesions showed responses comparable to sham-operated rats. These results indicate that a neural pathway important for fluid balance passes through, or terminates in, the nucleus medianus.
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PMID:Deficits in drinking and vasopressin secretion after lesions of the nucleus medianus. 688 60

The roles of oropharyngeal and gastric factors in satiation and arginine vasopressin (AVP) secretion were examined in water-deprived dogs. Dogs were prepared with chronic gastric fistulas and received six treatments after 24 h of water deprivation: rehydration with H2O or extracellular fluid (ECF) with the fistula closed; rehydration with H2O or ECF with the fistula open; gastric administration of H2O or ECF via the fistula. Drinking occurred immediately after presentation and was always completed by 6 min. At the end of the 60-min period of observation, water was offered in order to assess the degree of satiety. No differences were observed between the volumes of H2O or ECF consumed. However, only absorption of the water drunk produced complete satiety assessed 60 min later. Drinking H2O caused a fall in plasma AVP 6 min before a detectable decline in osmolality and reached water-replete levels by 15 min after drinking. Drinking H2O or ECF plus removal via the fistula and drinking ECF also brought about a rapid decline in plasma AVP without any change in plasma osmolality. Gastric administration of H2O caused a fall in plasma AVP that coincided with the fall in osmolality, and gastric administration of ECF had no effect on plasma AVP. We conclude that oropharyngeal factors account for temporary satiety and the rapid inhibition of vasopressin secretion.
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PMID:Satiety and inhibition of vasopressin secretion after drinking in dehydrated dogs. 701 97

Six dogs were administered third ventricular infusions of artificial cerebrospinal fluid (CSF) (292 mosmol/l) alone or artificial CSF to which neither NaCl, sucrose, glucose, or urea was added to yield a final osmolar concentration of 500 mosmol/l. The volume of water drunk during 45 min of infusion was measured and blood was sampled for determination of plasma vasopressin concentration at 15-min intervals. Artificial CSF made hypertonic by addition of NaCl or sucrose stimulated water intakes of 9.0 +/- 3.2 ml/kg (mean +/- SE) and 7.3 +/- 3.7 ml/kg, respectively. There was no statistical difference in the amounts drunk and the latencies. In contrast, artificial CSF containing glucose, urea, or artificial CSF alone were without effect. Plasma vasopressin concentration increased significantly in response to intraventricular NaCl and sucrose but was not affected by glucose, urea, or artificial CSF alone. These data are compatible with an osmoreceptor mechanism mediating drinking and vasopressin release.
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PMID:Drinking and vasopressin release during ventricular infusions of hypertonic solutions. 737 73

Controversial results of fluid and electrolyte derangements in patients with moderate alcohol intoxication have been described. However, no information is available about severe alcohol intoxication. We investigated differences of hormonal disorders between alcohol-habituated and alcohol-naive subjects with severe ethanol intoxication. The hormonal derangements and recommendations on therapy of these patients are discussed. Thirty-three patients [10 alcohol-naive (group A) and 23 alcohol-habituated (group B) subjects] with severe alcohol intoxication (blood ethanol > 200 mg/dl) were selected for the study. Electrolytes and osmolarity of serum and urine, blood ethanol, vasopressin, renin, and aldosterone were determined on admission 2, 4, and 6 hr later. Fluid balance was calculated for each hour. All patients received isotonic saline solution according to urine production. Group A: On admission, serum osmolarity was increased (308 mOsmol/kg). Concomitantly, vasopressin level was elevated on admission (9.12 pg/ml). Increased serum osmolarity was correlated with elevated vasopressin levels (r = 0.8211; p < 0.005). Serum electrolytes, renin, and aldosterone values were within normal ranges. Group B: On admission, vasopressin level was significantly decreased (0.9 pg/ml), despite an elevated serum osmolarity (309 mOsmol/kg). Serum osmolarity remained high despite a sufficient fluid substitution. In addition, vasopressin level remained suppressed over the observation period. Aldosterone level was significantly increased on admission (319 ng/ml). Accordingly, serum sodium was increased from 142 to 148 mM/liter, and serum potassium was decreased from 3.9 to 3.4 mM/liter. Response to hyperosmolarity due to severe alcohol intoxication is different in alcohol-naive and alcohol-habituated subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hormonal derangements in patients with severe alcohol intoxication. 794 88

Disturbances in homoeostatic capacity are typical of the ageing process. Changes in the neuroendocrine controls of salt and water homoeostasis with age make elderly people more susceptible to fluid and electrolyte disturbances such as dehydration and overhydration. Not only do elderly subjects show reduced thirst and water intake following dehydration, but their kidneys are less able to retain water. This reduced thirst and water intake is not dependent on palatability of the liquids offered as the amounts drunk are no different if water alone or a variety of beverages are offered to healthy elderly dehydrated men. It is of interest that the arginine vasopressin (AVP) response to dehydration is maintained in elderly subjects, indicating that their reduced renal water retentive capacity is due to relative renal resistance to vasopressin. The mechanism underlying the reduced thirst is unclear. Dehydration causes plasma hypertonicity and reduced extracellular fluid (ECF) volume, both of which stimulate thirst and AVP secretion. Elderly subjects show deficits in sensing the reduced ECF volume through reduced low and high pressure baroreceptor sensitivity. In contrast, while the AVP responses to hypertonicity are maintained, the thirst responses seem to be reduced. It seems unlikely that the primary sensing 'osmoreceptor' neurons in the hypothalamus leading to AVP secretion or thirst would be differentially affected by age. Therefore the thirst deficit may result from changes with age in the more poorly defined pathways that bring thirst to consciousness. Following rehydration, thirst and AVP secretion are inhibited in young individuals thus avoiding overhydration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Disturbed fluid and electrolyte homoeostasis following dehydration in elderly people. 843 52

We investigated the effect of ruminal water loading before feeding on the natriuretic and drinking responses that follow feeding. Six sheep fed 800 g of chaff drank 1360 +/- 150 mL during the 5 h immediately following feeding and increased renal Na excretion. Plasma Na concentration increased by 4 mmol L (-1) and plasma osmolality by 9 mosmol kg (-1) within 1.5 h and remained elevated. A rumen load of water administered before feeding prevented the increases in plasma Na and osmolality without affecting feeding. The natriuresis, water drinking and vasopressin secretion in response to feeding were abolished. Total sodium excreted during the experiment was halved in water-loaded animals compared with untreated animals (30.4 +/- 2.1 mmol (-1) cf. 63.8 +/- 2.9 mmol-1; P < 0.01). Ruminal loading with isotonic saline caused a 33% reduction in postprandial drinking, however, reducing cerebrospinal fluid NaCl concentration abolished postprandial drinking and natriuresis. Intravenous infusion of isotonic dextran appeared to delay the onset of water intake without changing the total volume of water drunk, suggesting a role of plasma volume in initiating drinking. We conclude from the data that central osmoregulatory mechanisms that include increased sodium excretion as well as thirst and vasopressin release are activated following food intake by sheep.
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PMID:Influence of ruminal water-loading on renal sodium excretion and water intake following feeding in sheep. 1144 55


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