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)

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.
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PMID:Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats? 5 84

Slices from ox neurohypophyses were incubated in a calcium-free medium with the ionophores A23187 or X537A. X537A (5 X 10(-5) mol/l) caused a marked release of vasopressin, neurophysin and protein to the medium. A23187 (2 X 10(-5) mol/l) did not cause any release by itself, but when Ca2+ was added to the medium in the presence of the ionophore, an increase in the release of vasopressin, neuorphysin and protein occurred. Release of lactate dehydrogenase and peptidase were not affected by the ionophores. The secretion caused by A23187 was abolished by D600 (a verapamil analogue) (2 X 10(-5) mol/l) whereas the effect of X537A was unchanged. The effects of X537A were strongly inhibited by removal of sodium from the medium. Re-addition of sodium to the medium caused a marked release. Gramicidin (10(-6) or 5 X 10(-5) mol/l) had no effect on secretion. Efflux of 45Ca2+ from pre-loaded slices was drastically reduced in a sodium-free medium. X537A caused an increase in the efflux rate of 45Ca2+ both in medium with a normal concentration of sodium and when slices had been incubated in a sodium-free medium. A23187 and X537A both released 45Ca2+ from a neurohypophyseal mitochondrial fraction. When sodium in a concentration of 20 mmol/l was added to this fraction, the Ca2+ accumulation was inhibited. This effect was reduced by inorganic phosphate up to a concentration of 2 mmol/l.
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PMID:Calcium and stimulus secretion coupling in the neurohypophysis. V. The effects of the Ca2+ ionophores A23187 and X537 A on vasopressin release and 45Ca2+ efflux; interactions with sodium and a verapamil analogue (D600). 6 Aug 66

Administration of pituitrin, vasopressin, and oxytocin to rats during spontaneous micturition increases diuresis and sodium excretion by reducing tubular reabsorption. In adrenalectomized rats these preparations have no diuretic effect and increased sodium excretion is observed only after administration of vasopressin. After hypophysectomy the diuretic effect of the preparations disappears but they still increase sodium excretion. It is postulated that the diuretic effect of the neurohypophyseal hormones is connected with activation of the pituitary-adrenal system, whereas some additional mechanism is involved in their effect on sodium excretion.
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PMID:Mechanism of action of neurohypophyseal hormones on sodium excretion and diuresis. 6 76

The concept of the "inappropriate" has a well-defined and easily comprehended meaning when applied to tumour secretion of antidiuretic hormone (A.D.H., vasopressin). When applied to high A.D.H. in other situations such as nephrotic syndrome, congestive cardiac failure, or cirrhosis, the use of the term "inappropriate secretion" simply reflects the fact that an easily measured controlling factor (plasma tonicity) is being overridden by a less easily measured one (effective extracellular volume). Similarly, sodium excretion in hypertension is said to be inappropriately low for the raised renal perfusion pressure: in this case inappropriateness results from the antinatriuretic effect of a minor degree of sodium depletion produced by pressure natriuresis. A similar objection can be made to the application of the term to the relations between renin or angiotensin-II concentrations and blood-pressure in some forms of hypertension. Since inappropriateness merely reflects the position and predilections of the observer, the widespread use of the term should be abandoned.
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PMID:On the inappropriate in hypertension research. 7 8

17 patients with severe hyponatraemia (none had cardiac failure or had lately had an operation) all had excessively high plasma-antidiuretic hormone (A.D.H.). Only 13 had features typical of the syndrome of inappropriate secretion of A.D.H. (S.I.A.D.H.). Plasma-A.D.H. was not related to either plasma-sodium or diagnosis. There were as many patients with chest infection as with carcinoma of the lung. Plasma-sodium and plasma-A.D.H. returned rapidly towards normal in the patients with chest infection or volume depletion but these concentrations corrected much more slowly in patients with carcinoma of the lung. The increase in plasma-sodium in patients with chest infection was too rapid to be produced by water-deprivation treatment and was due to return of plasma-A.D.H. to normal. The term S.I.A.D.H. implies an understanding of pathophysiology that does not exist. As a diagnosis it does not help in management or prognosis. A simpler, more descriptive terminology such as "hyponatraemia with carcinoma of the lung" would be more useful and less confusing in the clinical situation.
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PMID:Severe hyponatraemia. A study of 17 patients. 7 64

A study has been conducted to determine the ionic and metabolic requirements for full expression of the hydroosmotic response to antidiuretic hormone in the toad urinary bladder. By appropriate manipulation of incubation conditions it can be shown that there is a pool of serosal sodium necessary for a full hormone response. This serosal sodium pool is not related to the transepithelial sodium transport pool A full hydroosmotic response also requires serosal potassium; however, no specific anion requirement was demonstrated. Additionally, anaerobic or aerobic metabolism support a full hydroosmotic response equally well.
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PMID:Ionic and metabolic requirements for the hydroosmotic response to antidiuretic hormone in toad urinary bladder. 9 87

Two patients with the syndrome of inappropriate secretion of antidiuretic hormone were studied in a metabolic ward during treatment with 1.2 g demeclocycline daily. In both patients, demeclocycline treatment led to increased renal water excretion with consequent correction of hyponatremia and hypo-osmolality. Three episodes of reversible deterioration in glomerular filtration rate developed in these patients. Each episode was accompanied by clinical evidence of extracellular fluid volume contraction, and on each occasion there was an inappropriate natriuresis with daily urinary sodium excretion remaining above 50 mEq. Although demeclocycline effectively reverses the electrolyte abnormalities of this syndrome, the potentially dangerous side effects that may develop exclude the routine usage of the drug.
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PMID:Renal function during treatment of inappropriate secretion of antidiuretic hormone with demeclocycline. 10 Apr 73

A patient with the syndrome of inappropriate antidiuretic hormone release (SIADH) following head injury and meningitis was studied during treatment with demeclocycline, a drug known to produce a reversible nephrogenic diabetes insipidus. No changes were observed during six days of demeclocycline 1200 mg/24 hr but urine output increased significantly, with the production of a dilute urine, when the dose was increased to 2400 mg/24 hr. The patient lost weight, and all biochemical features of the syndrome were rapidly corrected despite an unchanged fluid intake and despite the persistence of high plasma levels of ADH. The rise in serum sodium was accompanied by mild sodium retention, as measured by external balance and exchangeable sodium. A complication of treatment was the development of acute renal failure possibly induced by a nephrotoxic effect of high circulating levels of demeclocyline. On stopping demeclocyline renal function returned to normal and, after some delay, SIADH returned, and was still present 9 months after initial presentation. This confirms earlier reports of the efficacy of demeclocycline in SIADH; but the authors advise caution against increasing the dose above 1200 mg/24 hr.
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PMID:Demeclocycline in the treatment of the syndrome of inappropriate antidiuretic hormone release: with measurement of plasma ADH. 10 83

The effects of the antidiuretic hormone (ADH) on the renal excretion of urea and electrolytes were studied in sheep, subjected to water stress, before and after 36-hour fasting. The intravenous administration of synthetic lysine-vasopressin (L-VP) at the dose of 100 microgram per kg induced only a temporary, statistically insignificant, drop of the urinary urea outputs by the fed as well as fasting sheep. L-VP did not influence the excretion of sodium and potassium electrolytes either. It follows from the results that there are no differences in the renal response to ADH between the fed sheep and sheep that have fasted for 36 hours.
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PMID:[The effect of the antidiuretic hormone on the renal excretion of urea and electrolytes in fed and fasting sheep]. 10 79

A patient with a syndrome of inappropriate antidiuretic hormone secretion secondary to an undifferentiated bronchogenic carcinoma with distant metastases was treated with demethylchlortetracycline. Up until recently, treatment of this syndrome was based on water restriction and when the plasma sodium concentration became extremely low, hypertonic saline solution administration. Recently it has been demonstrated that the antibiotic demethylchlortetracycline inhibits the action of the antidiuretic hormone on the renal tubules. The drug has been used successfully in five patients with the syndrome of inappropriate antidiuretic hormone secretion. The administration of 900 mg of demethylchlortetracycline per day for 7 days in our patient produced an increase of free water clearance, diuresis, plasma sodium concentration, and plasma osmolarity. Urinary excretion of sodium and urinary osmolarity declined. Furthermore, the neurological symptoms attributed to hyponatremia improved markedly. The patient lost 6 kg during treatment, probably because of negative water balance induced by demethylchlortetracycline. Even though the administration of demethylchlortetracycline did not produce significant decreases in the glomerular filtration rate or renal blood flow in our patient, it is advisable to control the renal function in individuals treated with this drug since it may on occasion determine renal insufficiency.
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PMID:[Treatment of the syndrome of inappropriate antidiuretic hormone secretion with demethylchlortetracycline (author's transl)]. 11 37


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