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)

Two patients with sodium-losing renal disease were studied in detail. Both presented with shock and hypotension which was attributed at first to other causes, as was the recurrent hyponatraemia in one of them. In both patients the cause of the sodium loss was probably unrelieved urinary obstruction which has been reported previously to cause water loss but not sodium loss. Both patients had severe hyponatraemia when they were sodium depleted, which has previously been attributed to water retention from excessive secretion of antidiuretic hormone. Plasma arginine vasopressin concentrations were raised in one patient but not in the other. The cause of the water retention in the other patient is not known. One of the patients, like others described in the literature, was only able to vary his sodium excretion within narrow limits. He became sodium depleted on a normal intake and oedematous when he was given saline intravenously. We suggest that the term sodium-losing renal disease should be replaced by the term 'fixed sodium' excretion renal disease.
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PMID:Sodium losing renal disease: Two cases and a review of the literature. 67 48

Lower body negative pressure (9-12 kPa) was applied to ten normal subjects. Large increases in plasma arginine vasopression concentration occurred only in subjects that experienced syncopal symptoms and developed hypotension. Blood samples obtained from the superior vena cava at 1/2 min intervals during application of negative pressure showed that maximal plasma vasopressin concentrations occurred with hypotension. Chromatography of the presyncopal plasma on Sephadex G-25 gave a large peak which eluted in the position of synthetic arginine vasopressin.
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PMID:Influence of lower body negative pressure upon arginine vasopressin release. 67 6

The effects of a synthetic analogue of vasopressin, DDAVP (1-deamino-8-D-arginine vasopressin) were investigated in 98 patients with cranial diabetes insipidus. In all patients, intranasal administration of DDAVP one to three times daily, usually twice daily, was found to be satisfactory in the control of diabetes insipidus. Thus, by DDAVP administration, daily urinary volume changed from 3520 +/- 2150 ml to 1620 +/- 830 ml (mean +/- SD), and urinary osmolarity changed from 126 +/- 75 mOsm/kgH2O to 446 +/- 194 mOsm/kgH2O (mean +/- SD). A daily dose of DDAVP ranged from 2.0 to 20 microgram in children (average dose 12.8 microgram), while 10 to 20 microgram of DDAVP was usually required in adult patients (average dose 14.2 microgram). No serious side effects have been observed. It is concluded that DDAVP is safe and effective in the treatment of cranial diabetes insipidus.
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PMID:[The treatment of patients with diabetes insipidus by a synthetic analogue of vasopressin, DDAVP (author's transl)]. 68 12

The effect of lowering the pressure of oxygen from 80 to 34 mm Hg was examined in anesthetized dogs that were undergoing a water diuresis. This degree of hypoxia was associated with an antidiuresis as urine osmolality (Uosm) increased from 107 to 316 mosmol/kg H(2)O (P < 0.001) and plasma arginine vasopressin increased from 0.06 to 7.5 muU/ml, (P < 0.05). However, hypoxia was not associated with significant changes in cardiac output (CO, from 4.2 to 4.7 liters/ min), mean arterial pressure (MAP, from 143 to 149 mm Hg), glomerular filtration rate (GFR, from 46 to 42 ml/min), solute excretion rate (SV, from 302 to 297 mosmol/min), or filtration fraction (from 0.26 to 0.27, NS). Hypoxia was associated with an increase in renal vascular resistance (from 0.49 to 0.58 mm Hg/ml per min, P < 0.01). The magnitude of hypoxia-induced antidiuresis was the same in innervated kidneys and denervated kidneys. To further examine the role of vasopressin in this antidiuresis, hypoxia was induced in hypophysectomized animals. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in hypophysectomized animals was the same as in intact animals. In contrast to intact animals, however, hypoxia did not induce a significant antidiuresis in hypophysectomized animals (Uosm from 72 to 82 mosmol/kg H(2)O). To delineate the afferent pathway for hypoxia-stimulated vasopressin release, hypoxia was induced in dogs with either chemo- or baroreceptor denervation. The effect of hypoxia on CO, MAP, GFR, SV, and renal blood flow in the denervated animals was the same as in nondenervated animals. Hypoxia resulted in an antidiuresis in chemoreceptor (Uosm from 113 to 357 mosmol/kg H(2)O, P < 0.001) but not in baroreceptor (Uosm from 116 to 138 mosmol/kg H(2)O, NS) denervated animals. To determine if hypoxia alters renal response to vasopressin, exogenous vasopressin was administered to normoxic and hypoxic groups of dogs. The antidiuretic effect of vasopressin was no different in these two groups. These results demonstrate that hypoxia induces an antidiuresis which is independent of alterations in CO, MAP, SV, filtration fraction, renal nerves, or renal response to vasopressin and occurs through baroreceptor-mediated vasopressin release. The nature of the baroreceptor stimulation remains to be elucidated.
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PMID:Mechanism of effect of hypoxia on renal water excretion. 70 76

Hypophysectomy caused an increase in superior mesenteric arterial conductance that reached a new plateau approximately 20 min after removal of the gland in four pentobarbital-anesthetized cats. Intravenous infusion of arginine vasopressin (0.74 +/- 0.21 mU min-1kg-1) caused conductance to decrease to approximately prehypophysectomy control values. Stopping the infusion resulted in an increase in conductance and the time course of this vasodilatation was virtually identical to that which occurred following hypophysectomy. The results are consistent with the interpretation that the effects of acute hypophysectomy on the mesenteric resistance vessels are due primarily to removal of the vasopressin system and the concomitant elimination of circulating vasopressin.
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PMID:Time course of mesenteric vasodilatation following hypophysectomy and the stopping of a vasopressin infusion. 70 14

Cerebral lesions involving most of the anterior wall of the ventricle, and the medial part of the septal region, induced a permanent loss of thirst in two goats. The ventral part of the lamina terminalis remained intact in one of the animals. Pronounced dehydration (10--13% loss of b.wt.) developed during periods (3--7 days) when water supplementation was omitted. Determinations of plasma arginine vasopressin in one of the animals revealed that the dehydration did not cause any significant increase in the secretion of antidiuretic hormone. However, the water deficit induced a considerable rise in plasma renin activity and tachycardia. If anything, the caroitid blood pressure became slightly elevated towards the end of 7 d dehydration periods. The lesions obviously inactivated a cerebral sensory mechanism controlling water balance. It may have been due mainly to destruction of juxtaventricular receptors in the anterior hypothalamic region, but perhaps also to a disruption of afferents from such receptors located posterior to this cerebral level.
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PMID:A study of permanent adipsia induced by medial forebrain lesions. 71 67

On the assumption that the antagonism between prostaglandin E2 and vasopressin might represent a negative feedback system, we evaluated the hypothesis that vasopressin stimulates, in vivo, the renal production of prostaglandins. For these studies we used Brattleboro homozygous rats with diabetes insipidus and Long-Evans rats for controls, Brattleboro homozygotes show a substantial reduction in the renal excretion of prostaglandin E2 and prostaglandin F2alpha. Homozygotes excreted 39 +/- 5 ng/24 h prostaglandin E2 and 40 +/- 4 ng/24 h prostaglandin F2alpha, compared to 217 +/- 40 and 221 +/- 18 ng/24 h, respectively, in control rats (P less than 0.001). Therapy of homozygotes with vasopressin tannate in oil resulted in a prompt increase in the urinary excretion of prostaglandin E2 and prostaglandin F2alpha. 1-Desamino-D-arginine vasopressin, a nonpressor analogue of vasopressin, also enhanced the renal production of prostaglandin E2. We conclude that vasopressin (antidiuretic hormone) stimulates renal production and excretion of prostaglandin E2 and prostaglandin F2alpha in vivo. It is possible that this increment of prostaglandin synthesis serves a negative feedback function by modulating the action of vasopressin on the renal tubule.
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PMID:Renal excretion of prostaglandins E2 and F2alpha in diabetes insipidus rats. 73 21

Impaired excretion of a water load is known to occur in adrenal insufficiency and to be corrected by administration of glucocorticoid. Such impairment has been related to either a loss of a permissive effect of glucocorticoids on the diluting segments of the nephron or to an alteration of release, turnover, or action of antidiuretic hormone. Specific and sensitive RIAs for arginine vasopressin and neurophysin were utilized to measure plasma and pituitary levels of neurohypophyseal peptides at baseline and after an intragastrically administered water load. Conscious, unanesthetized, and nonstressed sham-operated, adrenalectomized, and adrenalectomized prednisone-treated rats were studied. The results demonstrate a significant elevation in vasopressin and neurophysin in plasma in adrenalectomized rats maintained in a normal state of hydration. After water loading, the adrenalectomized rats diluted their plasma osmolality but had a decreased urinary volume, increased urinary osmolality, and elevated vasopressin and neurophysin in their plasma. In the pituitary, vasopressin and neurophysin were depleted in adrenalectomized rats, indicating increased secretion of these peptides. It is concluded that elevated vasopressin in plasma may be an important factor in the incomplete water diuresis in adrenal insufficiency.
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PMID:Plasma neurophysin and vasopressin in the rat: response to adrenalectomy and steroid replacement. 74 29

Sensitive and highly specific RIAs for arginine vasopressin (AVP) and oxytocin (OT) were utilized to assess the specificity of neurohypophyseal hormone release after hemorrhage or infusion of hypertonic saline to trained conscious dogs. Phlebotomy of 12.5 and 25 ml/kg produced increases in plasma AVP from 1.0 +/- 0.2 to 7.8 +/- 2.1 and 41.6 +/- 9.7 (SEM) microunit/ml respectively, and both responses differed significantly from values in control experiments (P less than 0.01 after the first phlebotomy and P less than 0.001 after the second phlebotomy). Plasma OT concentrations rose from baseline values of 1.1 +/- 0.4 to 3.3 +/- 0.6 and 8.3 +/- 1.7 microunit/ml (P less than 0.005 and P less than 0.001 compared to controls); plasma osmolality and sodium concentrations were unchanged. Both log AVP and log OT were highly correlated with the quantity of blood removed (r = 0.92 and -0.82, each P less than 0.001). Infusion of hypertonic (20g/dl) NaCl (3.4 meq/kg) over 20 min caused plasma osmolality and sodium to rise from 304 +/- 1.0 mosm/kg and 143 +/- 3.0 meq/liter to 316 +/- 1.0 mosm/kg and 150 +/- 3.0 meq/liter (each P less than 0.001). Plasma AVP rose from 1.5 +/- 0.2 to 2.4 +/- 0.2 microunit/ml (P less than 0.0025) and OT rose from 1.2 +/- 0.5 to 2.6 +/- 0.7 microunit/ml (P less than 0.005). The stimulus response ratios (change in log hormone concentration divided by the rise in plasma osmolality) were comparable for both hormones (0.024 +/- 0.006 for AVP and 0.031 +/- 0.008 for OT; P less than 0.4). The data indicate that hemorrhage or hypertonic saline stimulate release of both AVP and OT. After hemorrhage, there is greater stimulation of AVP than OT, whereas there is comparable stimulation of both peptides after hypertonic saline.
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PMID:The effect of hemorrhage and hypertonic saline upon plasma oxytocin and arginine vasopressin in conscious dogs. 74 39

A synthetic vasopressin analog, 1-desamino-8D-arginine vasopressin (DDAVP also known as desmopressin), was found to be highly effective in the treatment of seven children and one adult with vasopressin-sensitive diabetes insipidus. The average duration of action of DDAVP was 10 to 11 hours, and with proper adjustment of dose, the subjects were able to control their symptoms satisfactorily with one or two inhalations daily. The youngest child in whom adequate control was achieved was 2 years of age. All subjects found the use of intranasal DDAVP superior to other forms of therapy, and none experienced any known side-effects after six months of treatment. All subjects in this study are currently using 2.5 mug to 10 mug of DDAVP once or twice daily.
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PMID:Vasopressin analog DDAVP in the treatment of diabetes insipidus. 76 13


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