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

Steep transmembrane concentration gradients in vascular smooth muscle for all ions are maintained by energy-requiring pumps. The Na+ gradient appears to dominate the distribution of the other ions primarily because it controls cell hydration and energizes the transport of sugars, amino acids, and Ca++, Mg++, and H+. The Na+ gradient is a closely regulated constant (about ten to one) and is not perturbed except by changes in the limited permeability of the vascular smooth muscle membrane to Na+ or in the activity of its transport enzyme, the Na+-K+ATPase. Increased permeability to Na+ has been seen in vascular smooth muscle and in erythrocytes in salt-dependent forms of experimental hypertension, as well as in essential hypertension. A compensatory increase in Na+ transport (extrusion) has been seen. This increase in transport can be produced by a moderate increase in aldosterone acting alone or by a lesser increase acting synergistically with vasopressin.
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PMID:Monovalent and divalent ions in vascular tissue. 630 75

The role of vasopressin as a pressor agent to the hypertensive process was examined. Vasopressin plays a major role in the pathogenesis of DOCA-salt hypertension, since the elevation of blood pressure was not substantial in the rats with lithium-treated diabetes insipidus after DOCA-salt treatment. Administration of DDAVP which has antidiuretic action but minimal vasopressor effect failed to increase blood pressure to the levels observed after administration of AVP. Furthermore, the pressor action of vasopressin appears to be important in the development of this model of hypertension, since the enhanced pressor responsiveness to the hormone was observed in the initial stage of hypertension. Increased secretion of vasopressin from neurohypophysis also promotes the function of the hormone as a pathogenetic factor in hypertension. An unproportional release of vasopressin compared to plasma osmolality may be induced by the absence of an adjusting control of angiotensin II forming and receptor binding capacity for sodium balance in the brain. However, the role of vasopressin remains to be determined in human essential hypertension.
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PMID:Vasopressin as a possible contributor to hypertension. 632 16

Measurements of the vasoactive hormones including norepinephrine, angiotensin II and arginine vasopressin, in patients with essential hypertension generally have revealed plasma levels which are considered to be in a subpressor range. The results of recent in vivo studies from our laboratory, however, suggest that norepinephrine, angiotensin II and vasopressin all increase blood pressure by enhancing calcium movement across plasma membranes of vascular smooth muscle. Thus, subpressor levels of these three hormones may interact to increase peripheral vascular resistance and increase blood pressure. In the present study the effect of a subpressor dose of norepinephrine, angiotensin II or vasopressin to potentiate the blood pressure response to a pressor dose of one of these vasoactive hormones was demonstrated in the conscious rat. Furthermore, the combined subpressor doses of two of these three hormones caused a significant rise in blood pressure, even though each hormone by itself did not alter blood pressure. These results therefore raise the possibility that the combined vascular effects of subpressor levels of these three vasoactive hormones might contribute to some, heretofore, unexplained, states of essential hypertension.
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PMID:Interrelationship between subpressor effects of vasopressin and other vasoactive hormones in the rat. 632 39

Renal and vascular prostaglandins, which are vasoactive factors with local action, are implicated in the regulation of arterial blood pressure and might play a role in the genesis of arterial hypertension. By their properties of supervision on intrarenal blood flow, on renin secretion, on excretion of electrolytes and on the antidiuretic action of vasopressin, the prostaglandins E2 and I2 of renal origin indirectly control the blood pressure balance. In patients suffering from essential hypertension the urinary excretion level of renal prostaglandins is normal or diminished. When given to patients in pharmacological doses, prostaglandins exert a marked hypotensive effect. Non steroidal antiinflammatory drugs who act through inhibition of the synthesis of prostaglandins combat the action on blood pressure of several antihypertensive agents and lower natriuresis normally induced by some diuretics. These data show the diversity of action of the prostaglandins. By these properties, prostaglandins take part in control mechanisms on arterial blood pressure and facilitate the therapeutic use in patients suffering from hypertension.
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PMID:[Prostaglandins and arterial pressure]. 635 69

In 22 50-year-old men with long-standing, untreated essential hypertension of the low renin type, venous plasma vasopressin concentrations were about three times those of 15 matched normotensive control subjects (p less than 0.005). These patients also had increased arterial concentrations of noradrenaline and adrenaline (p less than 0.05) but there was no direct association between these two catecholamines and vasopressin. On the other hand, adrenergic beta-receptor blockade with oxprenolol reduced both blood pressure and plasma vasopressin (p less than 0.01) while venous plasma dopamine concentrations significantly increased. In addition, the hypertensives had highly significantly increased serum uric acid (p less than 0.001) that correlated positively with venous vasopressin concentrations (p less than 0.05). According to these data, patients with the volume-sustained low renin type of essential hypertension have increased plasma vasopressin concentrations that probably are inversely related to dopaminergic nervous activity. The data also indicate that increased plasma vasopressin correlates with serum uric acid, most probably through increased tubular reabsorption of this acid.
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PMID:Increased plasma vasopressin and serum uric acid in the low renin type of essential hypertension. 636 68

In order to investigate the antidiuretic hormone (ADH) in essential hypertension and secondary hypertension, plasma ADH levels were measured in normal subjects, in patients with normal and low essential hypertension, and in other patients with various forms of secondary hypertension. Plasma ADH levels were significantly lower in low renin essential hypertension and higher in malignant hypertension than in normal subjects. The plasma ADH levels tended to be lower in renal hypertension and primary aldosteronism, and higher in renovascular hypertension, but these differences were not statistically significant. From these results, it appeared that ADH might play a role in malignant hypertension, but not in the other hypertensive diseases.
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PMID:Plasma antidiuretic hormone levels in patients with normal and low renin essential hypertension, and secondary hypertension. 636 8

A group of 89 individuals with essential hypertension was evaluated with several measurements including the neurophysin believed to be the human oxytocin neurophysin (OT-Np), and the human vasopressin neurophysin (VP-Np). The neurophysins are proteins synthesized within cells of the supraoptic and paraventricular nuclei in conjunction with their respective hormones oxytocin and vasopressin as part of a common precursor molecule and so may reflect the simultaneous presence in plasma of their associated hormones. A poor but statistically significant correlation was noted between levels of OT-Np and renin activity in plasma (PRA) either supine (r = 0.248) or erect (r = 0.255). Levels of OT-Np averaged 1.75 ng/ml and were inversely correlated with creatinine (r = -0.252), supine blood pressure (r = -0.450), plasma volume (r = -0.327), and 24-hour urine sodium (r = -0.313). Levels of Ot-Np could be suppressed by infusion of physiologic saline. Levels of OT-Np were lower in the volume expanded state and were positively correlated with the quantity of sodium excreted into a 24-hour urine collected after the infusion (r = 0.426) and inversely correlated with the supine systolic (r = -0.379) and supine diastolic (r = -0.455) blood pressures recorded after the infusion of saline. Oestrogen, a stimulus to the secretion of OT-Np, did not account for the elevation of OT-Np observed in the study, since mean levels of oestradiol (E2) in a subset of the patients with elevated OT-Np (E2 = 36 pg/ml) were not different from levels in subjects with lower values of OT-Np (E2 = 45 pg/ml).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Levels of the oxytocin-associated and vasopressin-associated neurophysins in plasma and their responses in essential hypertension. 637 63

103 patients with mild or moderately severe essential hypertension and 35 healthy normotensive subjects were examined. In all patients examined plasma osmolality, plasma renin activity and plasma level of vasopressin and aldosterone were estimated twice: first after administration of a diet with a sodium chloride content of 100 to 120 mmol/a day and 8 hours recumbency and a second time after 3 days of dietary sodium chloride restriction (20 mmol/a day) and 3-4 hours upright position. In hypertensives independent of the behaviour of the plasma renin activity similar values of the plasma osmolality, the plasma level of vasopressin and the aldosterone level could be established as in healthy persons. In contrast to normals in hypertensive subjects no significant correlation between plasma osmolality or plasma renin activity and plasma level of vasopressin and aldosterone was stated. In spite of normal levels of vasopressin and aldosterone a significant correlation between the plasma level of vasopressin and aldosterone and the systolic blood pressure was found in hypertensive patients. From the results obtained in this study follows that in hypertensive patients the plasma osmolality is only of secondary importance for the secretion of vasopressin and aldosterone and for the plasma renin activity. The importance of plasma vasopressin and aldosterone in the pathogenesis of hypertension seems to be probable but not yet unanimously proved.
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PMID:[Is there a relation between the renin-angiotensin-aldosterone system and vasopressin secretion in essential hypertension?]. 639 82

There is evidence for an increased secretion of vasopressin in most models of hypertension, e.g., deoxycorticosterone (DOC)-salt hypertension, one- and two-kidney renal hypertension, partial nephrectomy-salt hypertension, the spontaneously hypertensive rat (SHR), the Dahl salt-sensitive rat on a high-salt diet, and human essential hypertension. In most forms of hypertension, there is also an increased pressor responsiveness to vasopressin as well as to other pressor agents. Blockade of vasopressin with either a competitive antagonist or a specific antiserum lowered blood pressure substantially in DOC-salt hypertension, two-kidney, one-clip hypertension, the stroke-prone SHR with well-established hypertension, and the Dahl S rat treated with captopril. In rats with diabetes insipidus, one- and two-kidney renal hypertension, but not DOC-salt hypertension, can be produced. There is evidence that vasopressin can contribute to some models of hypertension as either a pressor or an antidiuretic agent.
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PMID:The role of vasopressin in hypertension. 669 Mar 29

In this study we found that, in 31 normal subjects, close to 90% of circulating arginine vasopressin (AVP), measured by radioimmunoassay, was associated with platelets. By using routine methods of centrifugation, which do not completely separate platelets, the normal range of plasma vasopressin was higher by twofold than the normal range in platelet-free plasma prepared by differential centrifugation, which was 1.4 +/- 1.0 sd pg/ml. Platelet vasopressin was 12.9 +/- 5.7 pg/ml. Patients with congestive heart failure had, on average, an elevated platelet-free plasma AVP, as did two patients with thrombocytopenia and one with thrombocytosis. Patients with essential hypertension had slightly high levels of platelet-free plasma AVP and demonstrated an abnormal inverse relationship between platelet-free plasma AVP and serum osmolality. Immunoreactive platelet vasopressin was slightly low in patients with essential hypertension and was subnormal in patients with congestive heart failure. These studies demonstrate that platelets normally present in centrifuged plasma cause an overestimation of the plasma vasopressin levels. Until the physiological meaning of plasma and platelet-bound AVP is understood, studies of circulating vasopressin should probably assess both plasma and platelet AVP levels.
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PMID:Plasma and platelet vasopressin in essential hypertension and congestive heart failure. 682 23


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