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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Overhydration inhibits release of vasopressin (VP) and oxytocin (OT) from the hypothalamo-neurohypophysial system during hypovolemia. We investigated whether opioid peptides mediate the inhibitory effect of water on secretion of these hormones. Conscious male rats were made hypovolemic by hemorrhage (HEM, 0.51 ml/min) of 20 and 35% of the blood volume or by injection of either subcutaneous polyethylene glycol (PEG, 20,000 mol wt, 35 ml/kg) or intraperitoneal histamine (HIS, 15 mg/kg, 1 ml/kg). Animals were intubated orally 1-4 min (HEM, HIS) or 6.75 h (PEG) later with or without administration of water (40 ml/kg). Four to seven min after intubation rats were injected with saline (1 ml/kg) or naloxone (2 or 5 mg/kg) and then decapitated 6-10 min later. Control animals were treated similarly but were not stimulated by hypovolemia. VP and OT were extracted from plasma and quantified by radioimmunoassay. Data were analyzed by analysis of variance. In HEM animals blood pressure fell and plasma osmolality increased, both of which correlated positively with the rise in plasma [VP] and [OT]. Overhydration lowered the plasma osmolality, attenuated the fall in blood pressure, and reduced [VP] and [OT] in plasma of HEM animals. The opiate receptor antagonist, naloxone, did not alter these changes in blood pressure or plasma osmolality, or the plasma [VP] after HEM in rats treated with or without water. Plasma [OT] was, however, increased by naloxone in both normally hydrated and overhydrated rats. Thus, regardless of the hydrational state of the animal, opioid peptides inhibited release of OT but not VP during hemorrhage. Data consistent with this interpretation were also obtained from rats made hypovolemic with PEG or HIS.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of VP and OT release by water in hypovolemia is independent of opioid peptides. 360 88

1. Intake and output of water, Na+ and K+ were measured in Long Evans and Brattleboro rats (deficient in hypothalamic and pituitary vasopressin) before and after subcutaneous injection of polyethylene glycol (PEG) sufficient to cause a substantial hypovolaemia. 2. In the Long Evans rats an initial fluid retention (due to oliguria and polydipsia) was accompanied by Na+ retention and K+ loss. On the second day there was a diuresis but Na+ retention persisted until days 3 and 4 when there was a natriuresis. 3. Brattleboro rats initially also showed fluid retention but this was achieved by hypodipsia with a greater oliguria; there was an accompanying retention of Na+ and K+. On the second day, a reduced fluid balance was still accompanied by Na+ retention but associated with kaliuresis. Diuresis and natriuresis occurred on the third day after PEG injection. 4. Thus, rats deficient in vasopressin respond to hypovolaemia by retaining fluid. The renal actions of aldosterone do not explain fully the changes in renal electrolyte handling.
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PMID:Fluid and electrolyte handling in Long Evans and Brattleboro rats following injection of polyethylene glycol. 362 39

The role of noradrenergic input to fluid balance regulatory systems in the anterior hypothalamus was studied by examination of norepinephrine (NE) turnover during reduction of systemic extracellular fluid volume. Extracellular fluid volume was decreased iso-osmotically by subcutaneous polyethylene glycol (PEG), known to increase thirst and vasopressin secretion. NE turnover was assessed by measuring the decline of NE concentration in brain micropunches after administration of alpha-methyl tyrosine in PEG- or sham-treated groups. Several hypothalamic areas were investigated, including the median preoptic area (MnPO), preoptic area (POA), paraventricular nucleus, supraoptic nucleus (SON), subfornical organ, ventromedial hypothalamus, and posterior hypothalamus. Volume-depleted animals showed significantly increased NE turnover in the MnPO, an important area for integration of fluid balance information. The POA and the SON also showed trends toward increased NE turnover. All other areas showed no difference in NE turnover between volume-depleted and normal animals. These results are consistent with previous findings that NE innervation to the MnPO is important in the control of fluid balance and also support the hypothesis that basal forebrain NE projections facilitate thirst and vasopressin secretion.
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PMID:Increased norepinephrine turnover in the median preoptic nucleus following reduced extracellular fluid volume. 367 14

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21

The intestinal transport of vasopressin and oxytocin and their analogues 1-deamino-8-D-arginine vasopressin and 1-deamino-2-tyrosine(omicron-ethyl)-oxytocin was studied in everted segments of rat jejunum. The transported peptides were identified by specific RIA methods and by quantitative high pressure liquid chromatography. Transport rates were highest for 1-deamino-8-D-arginine vasopressin and lowest for vasopressin. No transport maximum and no competitive inhibition could be demonstrated. The distribution volume of the peptides in the intestinal mucosa was found to be smaller than that of polyethylene glycol. It is concluded that peptides of this size are transferred across the intestinal mucosa by passive processes.
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PMID:In vitro intestinal transport of vasopressin and its analogues. 371 36

Regulation of posterior pituitary secretion of vasopressin (AVP) and oxytocin (OT) was studied in rats given electrolytic lesions of ventral nucleus medianus (vNM). As described previously, rats with such lesions were chronically hypernatremic and showed impaired drinking responses to an osmotic challenge. AVP secretion in response to osmotic stimuli also was significantly blunted, although sufficient increases in plasma AVP levels did occur, in association with an abnormally high range of plasma sodium concentrations, to allow urinary concentration comparable to control animals. These findings suggest that vNM lesions cause an upward resetting of the osmotic threshold for AVP secretion. In contrast, hypovolemia, produced by subcutaneous polyethylene glycol treatment, and hypotension, produced by phentolamine treatment, both evoked AVP responses in rats with vNM lesions that were equivalent to those seen in control animals. Plasma OT responses to osmotic and hemodynamic stimuli were analogous to the AVP responses. These findings reproduce the major clinical features observed in humans with the disorder of essential hypernatremia and by doing so support proposals that this disorder is caused by lesions in the vicinity of the anterior hypothalamus that result in selective destruction of afferent osmosensitive inputs to the neurohypophysis.
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PMID:Impaired secretion of vasopressin and oxytocin in rats after lesions of nucleus medianus. 407 88

Synthetic [8-arginine]-vasopressin, [8-lysine]-vasopressin, [8-ornithine]-vasopressin or [2-phenylalanine, 8-lysine]-vasopressin aggregated human platelets in heparinized platelet-rich plasma. The lowest effective concentrations (1-4mU/ml) caused a primary transient aggregation, while higher concentrations also caused a secondary irreversible aggregation. Vasopressin was almost inactive in citrated platelet-rich plasma but caused aggregation in recalcified citrated or native material. Vasopressin also aggregated washed human platelets suspended in buffered saline, if fibrinogen and either Ca2+ or Mg2+ ions were present. Ethylene glycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid inhibited aggregation completely but only after preincubation with the platelets, suggesting that platelet-bound calcium was also required. Phosphocreatine with creatine phosphokinase partially inhibited primary aggregation of platelets by vasopressin and prevented secondary aggregation, which suggests that release of platelet ADP contributed to these processes. Concentrations of vasopressin causing irreversible aggregation released small amounts of 14C from platelets containing serotonin-14C. Platelet aggregation induced by vasopressin was inhibited by adenosine, prostaglandin E1, N6,2'-0-dibutyryl cyclic 3',5'-AMP, caffeine, imipramine, or N-ethylmaleimide. Adenosine and prostaglandin E each inhibited the action of vasopressin much more powerfully than that of ADP and, therefore, cannot act solely by inhibiting the effects of the ADP released. In several respects the effect of vasopressin on blood platelets resembled its action on smooth muscle.
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PMID:Aggregation of human blood platelets by vasopressin. 434 80

Peptide hormones labelled with radioactive iodine were partitioned into the aqueous two-phase polymer systems developed by Albertsson (1960) and the conditions required for separation of free from antibody-bound hormone have been worked out. Hormones studied included insulin, growth hormone, parathyroid hormone and [arginine]-vasopressin. Free and antibody-bound hormones show different distribution coefficients in a number of systems tested; two systems, the dextran-polyethylene glycol and dextran sulphate-polyethylene glycol system, give optimum separation. Free hormones distribute readily into the upper phase of these systems, whereas hormone-antibody complexes, as well as uncombined antibody, are found almost completely in the lower phase. Various factors including the polymer concentration, the ionic composition of the system, the nature of the hormone and the nature of added serum protein differentially affect the distribution coefficients for free and antibody-bound hormone. These factors can be adequately controlled so as to improve separation. The two-phase partition method has been successfully applied to measure binding of labelled hormone to antibody under standard radioimmunoassay conditions. It exhibits several advantages over the method of equilibration dialysis and can be applied to the study of non-immunological interactions.
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PMID:Distribution of free and antibody-bound peptide hormones in two-phase aqueous polymer systems. 467 74

It is generally believed that urea crosses the cell membrane through aqueous channels, and that its movement across the membrane is accelerated in the direction of net water flow (solvent drag effect). The present report presents evidence for a vasopressin-sensitive pathway for the movement of urea, other amides, and certain non-amides, which is independent of water flow. Phloretin, when present at 10(-4) M concentration in the medium bathing the luminal surface of the toad bladder, strongly inhibits the movement of urea, acetamide, and propionamide across the toad bladder, both in the absence and presence of vasopressin. The vasopressin-stimulated movement of formaldehyde and thiourea is also reduced. Osmotic water flow, on the other hand, is not affected; nor is the movement of ethanol and ethylene glycol, or the net transport of sodium. On the basis of these studies we would conclude that the movement of many, if not all, solutes across the cell membrane is independent of water flow, and that a vasopressin-sensitive carrier may be involved in the transport of certain solutes across the cell membrane.
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PMID:Effect of phloretin on water and solute movement in the toad bladder. 470 29

Intracerebroventricular (i.v.t.) administration of beta-endorphin or leucine5-enkephalin inhibited drinking behavior, the pressor response and increased plasma vasopressin concentration stimulated by an acute elevation in CSF sodium chloride concentration (10 microliter, 1 M NaCl i.v.t.). These effects of endogenous opioid peptides were prevented by naloxone, indicating opiate receptors were required for the biologic response. Drinking behavior associated with regulatory stimuli operant during dehydration was also inhibited by opioid peptides. beta-Endorphin (i.v.t.) delayed the onset and/or reduced the volume of water consumed in response to hypertonic sodium chloride (relative cellular dehydration), polyethylene glycol (hypovolemia) and food-associated drinking behavior. Inhibition of drinking did not appear related to sensory-motor dysfunction as another motivated behavior, eating (onset, amount consumed) was unaffected by beta-endorphin. It is concluded from these results that centrally administered endogenous opioid peptides inhibit sodium chloride-stimulated cerebral mechanisms affecting blood pressure and hydration.
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PMID:Effects of centrally administered endogenous opioid peptides on drinking behavior, increased plasma vasopressin concentration and pressor response to hypertonic sodium chloride. 626 92


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