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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

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

Plasma concentrations of arginine-vasopressin (antidiuretic hormone) have been measured in 40 patients with benign essential hypertension and 12 patients with malignant-phase hypertension. Values tended to be low in the benign phase and high in the malignant phase. 5 normal subjects were infused with synthetic arginine-vasopressin, producing plasma concentrations up to five times the highest value recorded in malignant-phase hypertension, without any effect on blood-pressure. There is no evidence that vasopressin has a direct role in the pathogenesis of benign essential hypertension or its transition to the malignant phase. On the contrary, abnormal vasopressin concentrations may be caused by hypertension.
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PMID:Changes of vasopressin in hypertension: Cause or effect? 7 91

We investigated the role of arginine-vasopressin (AVP) in maintaining the blood pressure of spontaneously hypertensive (SH) rats (stroke-prone strain) with established hypertension (22--28 weeks of age). In comparison with normotensive Wistar Kyoto (WKY) rats, plasma AVP concentrations of SH rats with benign hypertension (BH) were elevated twofold and in rats with severe or malignant hypertension (S-MH), fourfold. The height of the blood pressure was quantitatively related to plasma AVP in both BH and S-MH rats, the overall correlation coefficient being 0.66 (p less than 0.001). The intravenous injection of a specific AVP antiserum into conscious and unrestrained rats lowered blood pressure in 4 BH rats by 48 +/- 14 mm Hg and in 4 S-MH rats by 78 +/- 10 mm Hg and had only a marginal effect in 4 normotensive WKY rats. Infusion of saralasin did not lower blood pressure in WKY and BH rats and reduced blood pressure in only 2 of 7 S-MH rats tetsted (by 15 and 20 mm Hg). During AVP infusion the blood pressure of SH rats increased more (p less than 0.001) and heart rate fell much less (p less than 0.001) than in WKY rats. It is concluded that in SH rats with established hypertension, plasma AVP plays an important role in the maintenance of high blood pressure, while the renin-angiotensin system plays a minor or no role.
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PMID:Studies on the role of vasopressin in blood pressure control of spontaneously hypertensive rats with established hypertension (SHR, stroke-prone strain). 9 26

Using Brattleboro rats with and without hereditary diabetes insipidus (DI, non-DI), blood pressure, water intake and the excretion of water, sodium, potassium and osmotically active substances were measured in intact individuals and in animals subjected to unilateral nephrectomy at the age of 23 or 80 days. The development of blood pressure (BP) changes, determined in unilaterally nephrectomized animals at the age of 4--6 months, depended on the age at which the kidney was removed. After nephrectomy at the age of 25 days, hypertension developed only in DI females given 0.6% NaCl solution to drink. The BP of those which drank water was unaffected. Unilateral nephrectomy at the age of 80 days produced a slight BP increase in females irrespective of whether they drank water or 0.6% NaCl, but in males only if they drank 0.6% NaCl solution. No hypertension was observed in intact animals. No relationship was found between water intake and the blood pressure level. The BP increase in water-drinking females uninephrectomized at 80 days was accompanied by a raised urine flow and raised excretion of osmotically active substances. Sodium losses in DI animals were greater than in non-DI animals and the urinary sodium concentration, in maximum dehydration, attained minimum values in DI and maximum values in non-DI animals. Unilateral nephrectomy at 25 days increased sodium losses in all the animals except non-DI females, but when performed at 80 days, only in DI males. No relationship between these results and BP changes was found. The possible relationship of the extrarenal consequences of absence of vasopressin to the development of experimental hypertension are discussed.
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PMID:Blood pressure and water and electrolyte intake and excretion in rats (Brattleboro strain) after unilateral nephrectomy. 14 74

A 16-month-old black male infant had unusual thirst, polyuria, hyponatremia, and hypertension. His polyuria was unresponsive to vasopressin therapy, and his high blood pressure was not effectively controlled by antihypertensive drugs. Radiographic examinations revealed an occult Wilms tumor in the right kidney. After removal of the tumor, the signs and symptoms were relieved. The tumor had a renin activity about 280 times that of the adjacent renal cortex, and many intracytoplasmic secretory granules were found on electron microscopy. The pathogenesis of these clinical manifestations appears to be mediated through the physiologic pathways of renin-angiotensin II and renin-aldosterone.
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PMID:Polydipsia, polyuria, and hypertension associated with renin-secreting Wilms tumor. 20 43

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.
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PMID:The role of vasopressin in blood pressure control and in experimental hypertension. 28 63

In acute gastrointestinal bleeding visceral angiography has been showing its importance for years. It contributes to diagnosis especially in cases with persistent acute hemorrhage. In chronic gastrointestinal bleeding conventional radiographic procedures such as upper gastrointestinal series and barium enema will be preferred to angiography. The function of the radiologist goes beyond mere diagnosis of gastrointestinal bleeding. Treatment with vasopressin via the angiographic catheter has proven its clinical value. This method will be indicated especially in cases with high risk anesthesia and surgery. It will help to postpone necessary surgery to a more favorable moment following hemostasis. Side effects such as hypertension and antidiuresis are relatively rare and easy to manage. Numerous substances are used for embolization showing that ideal material has not been found yet and further development seems necessary. In contrast to vasopressin treatment, vascular occlusion is often irreversible, complications (unwanted reflux of embolization material, necrosis and plugging of the catheter) are more difficult to manage. Superselective visualization of a bleeding artery is always needed. Embolization is justified in cases when a possibility for anesthesia and surgery cannot be foreseen. The electrical vascular occlusion using direct current is still in the phase of animal experiments; its clinical value has not sufficiently been assessed as yet.
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PMID:[Angiographic diagnosis and therapy of acute and chronic gastrointestinal hemorrhages]. 30 84

This review provides a summary and assessment of research involving renal prostaglandins. Arachidonic acid released from phospholipids is converted by prostaglandin cyclo-oxygenase in the kidney to PGF2, PGF2alpha, PGD2, and, possibly, to PGI2 and thromboxane A2. Production of PGE2 and PGF2alpha is predominately but not exclusively in the medulla, whereas degradative enzymes are present in both cortex and medulla. Prostaglandins enter the tubular lumen by facilitated transport and are partially reabsorbed from the urine in the distal nephron. Urine prostaglandins probably reflect renal synthesis. PGE2 and endoperoxides stimulate and PGF2alpha and indomethacin inhibit renal renin synthesis. In response to ischemia, vasoconstriction, or angiotensin II the kidney increases prostaglandin synthesis to modulate renal vascular resistance. In conscious animals or man no role has been established for prostaglandins in the maintenance of basal renal blood flow or renal sodium excretion. PGE influences renal water excretion by inhibiting the action vasopressin. Despite conflicting data there is evidence that renal prostaglandins are involved either primarily or secondarily in many types of hypertension. Inhibitors of prostaglandin cyclooxygenase have been used with success in Bartter's syndrome. Conflicting results in many areas of investigation may be resolved by the use of more accurate and reliable assays, careful handling of samples, and the use of urine to further investigate renal prostaglandin synthesis.
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PMID:Prostaglandins and the kidney. 33 46

Inferior mesenteric arterial blood flow was measured with an electromagnetic blood flowmeter in five anesthetized rhesus monkeys. The effects of vasopressin on this vasculature were determined to evaluate the optimal, safe concentration of this agent during its clinical application in the management of hemorrhagic lesions of the colon. Control flow was 29 +/- 3 (SE) ml min-1; aortic pressure was 124 +/- 4 mm Hg. Intraarterial injections of vasopressin, in doses ranging logarithmically from 5 X 10(-5) to 5 X 10(-2) U kg-1, caused dose-dependent decreases in flow. At the highest dose, vasopressin reduced flow by 50% and increased arterial pressure by 9 mm Hg. When infused, at a rate of 5 X 10(-3) U kg-1 min-1, vasopressin produced a significant and sustained reduction in inferior mesenteric arterial blood flow. Autoregulatory escape was not observed. At this rate, vasopressin increased arterial pressure 10 mm Hg, by the 6th minute of infusion. This hypertension was unaccompanied by significant bradycardia. After cessation of the infusion, flow gradually returned to control values over a period of minutes. These observations indicate that vasopressin is a potent constrictor in the inferior mesenteric arterial circulation of the monkey, and support the use of this agent to control lower intestinal bleeding in man. At a dose of 5 X 10(-3) U kg-1 min-1, vasopressin causes a significant reduction in flow without adverse systemic side effects.
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PMID:Influence of vasopressin on colon blood flow in monkeys. 40 50


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