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)

1. Six male beagle dogs with carotid loops were infused with sodium chloride solution (150 mmol/l; saline) during control observations followed by dopamine infusion at various rates. Arterial blood samples were drawn during the control period and at the end of each period of dopamine infusion for the measurement of plasma dopamine, noradrenaline, adrenaline, renin, angiotensin II, aldosterone, vasopressin, electrolytes and packed cell volume. Blood pressure and pulse were recorded throughout. 2. The rate of infusion and plasma dopamine levels were closely correlated (r = 0.99, P less than 0.001). Plasma dopamine levels two to 20 times basal values produced no significant change in any of the other variables measured; levels 200 times basal values caused a significant increase (P less than 0.05) in plasma renin concentration; levels 2000 times basal values were associated with significant increases (P less than 0.05) in plasma renin and angiotensin II, packed cell volume and blood pressure, without significant changes in other measurements. 3. Circulating dopamine is unlikely to be important in the control of sodium and water metabolism.
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PMID:Circulating dopamine: its effect on the plasma concentrations of catecholamines, renin, angiotensin, aldosterone and vasopressin in the conscious dog. 702 27

Verney's hypothesis of cerebral osmoreceptors controlling the renal excretion of water via vasopressin was reinvestigated in conscious trained dogs provided with bilateral skin loops containing the common carotid arteries. In multiple experiments in two dogs, bilateral intracarotid injections (0.25 ml. (kg b.wt.)-1 per artery in 10 s) of a hyperosmotic solution of sodium chloride (0.257 mol/l) during transient water diuresis failed to produce an antidiuretic response, although it is estimated that the injections elevated the osmolality of the carotid blood by 12-15%. In another 5 dogs, Bilateral intracarotid infusions of hyperosmotic saline (45 mumol.(kg b wt..min)-1 per artery for 10 min) during sustained water diuresis resulted in a 3% increase in jugular venous osmolality and an antidiuretic response without detectable changes in heart rate or mean arterial pressure. Equal intravenous hyperosmotic or intracarotid isosmotic infusions were not associated with antidiuretic response. Analysis of the concomitant concentrations of vasopressin in plasma fell short of supporting the hypothesis that the antidiuretic response to intracarotid hyperosmotic infusions was exclusively or mainly due to liberation of vasopressin, although the renal response could be mimicked by exogenous vasopressin. It is concluded that the present results-although discordant with several of Verney's results and assumptions-nevertheless support the concept of a cerebral solute receptor influencing the rate of renal water excretion.
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PMID:The relation between carotid solute concentration and renal water excretion in conscious dogs. 713 45

1. The role of arginine-vasopressin (AVP) in the maintenance of high blood pressure in rats with deoxycorticosterone acetate (DOCA) hypertension was investigated. 2. Plasma concentrations of AVP were significantly elevated in DOCa hypertensive rats compared with normotensive control rats, whether or not they received 1% sodium chloride solution or demineralized water to drink. 3. The specific antagonist of the vasopressor response to AVP, d(CH2)5VDAVP (100 microgram/kg intravenously), significantly increased cardiac output and decreased total peripheral resistance, but had no effect on mean arterial pressure in DOCA hypertensive rats. No changes of mean arterial pressure, cardiac output and total peripheral resistance were observed in the normotensive control groups after d(CH2)5VDAVP. 4. After sino-aortic baroreceptor deafferentation, d(CH2)5VDAVP decreased mean arterial pressure in DOCA--salt hypertensive rats, but not in the control groups. 5. It is concluded that elevated circulating AVP causes vasoconstriction in DOCA hypertensive rats. The AVP-induced increase in total peripheral resistance is counter-regulated by an activation of the baroreceptor reflex and subsequent reduction in cardiac output.
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PMID:Vasopressin-induced increase in total peripheral resistance in deoxycorticosterone acetate hypertensive rats is buffered by the baroreceptor reflex. 718 84

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.
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PMID:Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action. 739 71

Normotensive anephric rats infused with 2 milliliters of a hyperosmolar solution of either sodium chloride or mannitol showed an increase in arterial pressure that was very pronounced with the sodium chloride and that could be partly abolished by administration of an antagonist to the vasopressor action of antidiuretic hormone (ADH). Rats with congenital ADH deficiency subjected to the same treatment showed smaller increments in arterial pressure that remained unchanged after administration of the ADH antagonist. Expansion of intravascular fluid volume was similar in all four groups and bore no correlation to the change in arterial pressure. It is concluded that about half of the increase in blood pressure induced by saline was attributable to the vasopressor effect of stimulated ADH and the remainder to an additional sodium-related factor, since it was more pronounced in the saline-infused than in the mannitol-infused groups. Expansion of the intravascular volume per se could only account for a minimal part of the increment in pressure.
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PMID:Sodium-induced elevation of blood pressure in the anephric state. 740 61

The present study was undertaken to investigate the effect of osmotic constituents of the incubation media on angiotensin II stimulation of arginine vasopressin (AVP) release from the organ-cultured guinea pig hypothalamo-neurohypophyseal complex (HNC). As reported previously, the addition of angiotensin II caused a significant increase in AVP release from the explants of HNC incubating in the normal culture medium. The media made hyperosmolar with sodium chloride also significantly increased AVP release from the explants. The addition of angiotensin II to the hyperosmolar sodium chloride caused a further increase in AVP release from the explants of HNC. However, the response to angiotensin II was not significantly different among the explants incubating in the hyposmolar, the isosmolar and the hyperosmolar sodium chloride solutions, indicating separate pathways of angiotensin II and osmotic stimuli in AVP release. In contrast, the response of the explants to angiotensin II was markedly suppressed when they were incubated in the media made hyperosmolar with excess glucose. Furthermore, the hyperosmolar media of excess urea failed to influence the angiotensin II-stimulated AVP release from the explants. These results are compatible with the hypothesis that excess glucose has a specific suppressive effect on AVP release from the neurohypophysis.
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PMID:Effects of glucose and sodium chloride on the release of vasopressin in response to angiotensin II from the guinea pig hypothalamo-neurohypophyseal complex in organ culture. 745 48

The effect of prostaglandins (PGs) on arginine vasopressin (AVP) release was investigated using the male guinea pig hypothalamo-neurohypophyseal complex (HNC) in organ culture. The explants of HNC were used on the second day in culture. The culture medium containing PGE2 caused an increase in AVP release from the explants during a 10-min incubation period. AVP release was significantly increased at a PGE2 concentration of 2 X 10(-8) M or more. AVP release was increased in a dose-dependent manner. PGF2 alpha at concentrations of 1.4 X 10(-7) and 1.4 X 10(-6) M also increased AVP release significantly. The explants in the group treated with 7.4 X 10(-5) M indomethacin for 60 min before the experiment and throughout the experiment responded to 6.5 X 10(-8) M angiotensin II with a 166 +/- 42% increase in AVP release over control release. The response of explants to the addition of angiotensin II in this group was significantly lower (P less than 0.05) than that in the group not treated with indomethacin, which was 439 +/- 128% of the basal value (P less than 0.05). The release of AVP in the group treated with indomethacin was 120 +/- 15% of the basal value in response to a hypertonic solution of sodium chloride at 310 mosmol/kg H2O and was significantly lower (P less than 0.05) than that in the group not treated with indomethacin (203 +/- 30% of the basal value; P less than 0.005). However, indomethacin did not alter basic release of AVP. These results suggest that PGE2 and PGF2 alpha increase AVP release from the explants of HNC in organ culture, although PGF 2 alpha has a relatively weaker effect than PGE2, and PGs may modulate the regulation of AVP release in response to angiotensin II and osmotic stimulation.
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PMID:The effect of prostaglandins on the release of arginine vasopressin from the guinea pig hypothalamo-neurohypophyseal complex in organ culture. 746 Aug 17

The use of psychotropic drugs has been associated with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) in a number of case reports. SIADH is characterised by the sustained release of antidiuretic hormone (ADH) from the posterior pituitary. The patients have a reduced ability to excrete diluted urine, ingested fluid is retained, and the extracellular fluid expands and becomes hypo-osmolar. The cardinal signs are hyponatraemia, serum hypoosmolality and a less than maximally diluted urine. Common symptoms include weakness, lethargy, headache, anorexia and weight gain. These symptoms may be followed by confusion, convulsions, coma and death. The early symptoms are vague and nonspecific, and they may even mimic the symptoms of the psychiatric disorder itself. For antidepressants, the risk of SIADH seems to be highest during the first weeks of treatment. For antipsychotics, the risk seems to be more spread out in time. The causative role of the drug may sometimes be difficult to estimate, as even drug-free psychiatric patients, mostly those with schizophrenia, develop SIADH on the basis of psychogenic polydipsia. Smoking is another factor associated with the development of SIADH, and the risk may also increase with age. The acute treatment of SIADH induced by a psychotropic drug includes discontinuation of the drug as well as restriction of fluid intake. In cases with significant clinical symptoms, infusion of sodium chloride is recommended. After the acute management, it is useful to evaluate the causative role of the drug by performing a water loading test and/or drug rechallenge. If continued treatment with an antidepressant or antipsychotic is indicated, a drug with a different pharmacological profile should be chosen, and the serum sodium levels should be monitored closely. If treatment with the drug that caused SIADH must be continued, concomitant treatment with demeclocycline may reduce the tendency of hyponatraemia.
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PMID:Hyponatraemia and the syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by psychotropic drugs. 761 32

The present study was undertaken to examine vasopressin gene expression in response to a normal versus hypertonic sodium chloride (506 mOsm/kg H2O) intake for 7 days in Sprague-Dawley rats. The animals in both groups demonstrated precision in maintaining constancy of body fluid composition in spite of large differences in sodium and water intakes. Compared with the rats on a normal diet, chronic ingestion of hypertonic sodium chloride resulted in significant increases in total fluid intake (210 +/- 8 mL v 471 +/- 48 mL, P < 0.001) and total urine output (86 +/- 5 mL v 347 +/- 48 mL, P < 0.001), while glomerular filtration rate, hematocrit, serum urea nitrogen, creatinine, serum sodium, and plasma osmolality were unchanged. Without detectable changes in plasma osmolality or intravascular volume, vasopressin release from the pituitary, as measured by plasma and pituitary vasopressin concentrations (1.5 +/- 0.1 pg/mL v 5.9 +/- 1.5 pg/mL, P < 0.01 and 2.0 +/- 0.5 micrograms/pituitary v 0.86 +/- 0.1 micrograms/pituitary, P < 0.01, respectively), was increased in the animals ingesting hypertonic sodium chloride. In addition, vasopressin gene expression as measured by hypothalamic vasopressin mRNA concentrations was significantly increased 1.85-fold (P < 0.001) in the animals ingesting hypertonic sodium chloride. In summary, Sprague-Dawley rats ingesting hypertonic sodium chloride (506 mOsm/kg H2O) were able to maintain sodium and water homeostasis over a 7-day period. Yet, in these animals plasma vasopressin increased, pituitary vasopressin stores decreased, and hypothalamic vasopressin gene expression was stimulated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic hypertonic saline ingestion on vasopressin gene expression in the rat. 768 41

Rats drinking ad libitum tap water or hypertonic (i.e. 2%) sodium chloride solution were given intracerebroventricularly (i.c.v.) for three days, thyrotropin-releasing hormone (TRH) in a daily dose of 200 ng dissolved in 10 microliters of 0.9% sodium chloride. Treatment with TRH resulted in significantly increased hypothalamic vasopressin content in both euhydrated (i.e. given tap water ad libitum) and salt-loaded rats. In rats given hypertonic saline, neurohypophysial vasopressin content increased. Plasma vasopressin concentration was distinctly diminished under TRH treatment, the respective difference being significant, however, barely in salt-loaded rats. The present data suggest that TRH may be involved in some regulatory processes related to vasopressin biosynthesis and release from the rat hypothalamo-neurohypophysial system.
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PMID:Thyrotropin-releasing hormone (TRH) inhibits vasopressin release from hypothalamo-neurohypophysial system of rats drinking hypertonic saline. 800 5


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