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)

The influence of tetrandrine on arterial pressure and heart rate of pentobarbitone-anaesthetized and conscious normotensive and hypertensive rats (SH rats, renal hypertensive rats, DOCA-salt hypertensive rats) was investigated. Tetrandrine administered intravenously (i.v.) to these animals caused an acute, long-lasting and dose-dependent decrease in mean arterial pressure. Heart rate was not significantly altered. In pithed rats, tetrandrine injected intraarterially 15 min previously impaired the increase in diastolic pressure induced by i.v. B-HT 920, a highly selective alpha 2-adrenoceptor-stimulating agent, in a dose-dependent manner. In a low dose, a parallel displacement to the right was observed, whereas for higher doses the shift was non-parallel. A high dose of tetrandrine shifted the pressor response curve of the alpha 1-adrenoceptor agonist, methoxamine, only slightly to the right and did not depress the maximal response. Tetrandrine also caused a moderate rightward shift of the vasopressor effect curve of vasopressin applied i.v. Tetrandrine displayed only minor affinities for specific binding sites in rat brain membranes for [3H]-prazosin (alpha 1-adrenoceptors) and for [3H]-clonidine (alpha 2-adrenoceptors). The results obtained suggest that the hypotensive effect of tetrandrine may be related to an impairment of vasoconstrictor tone mediated by vascular postsynaptic alpha 2-adrenoceptors.
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PMID:Hypotensive activity of tetrandrine in rats. Investigation into its mode of action. 630 16

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

A possible role for vasopressin in the development and/or maintenance of DOCA hypertension in pigs was studied. In control pigs mean arterial blood pressure (MABP), plasma lysine vasopressin (LVP) concentration, the 24-h urinary excretion of LVP (ULVPV) and plasma renin activity (PRA) did not change throughout the 30 days of the experiment. In DOCA-treated pigs MABP began to increase from the initial level of 95 +/- 2 mm Hg within 5 days and reached a level of 127 +/- 3 mm Hg between days 20-30 (P less than 0.01). At this time in the DOCA treated pigs, ULVPV increased threefold (P less than 0.05), although PLVP was unchanged and PRA was reduced to almost zero. After 30 days the pigs were fed a low sodium diet. This was without effect on MABP, PLVP and ULVPV in control pigs. However, in the DOCA-treated pigs, MABP fell from 133 +/- 2 to 112 +/- 6 mm Hg, accompanied by a 60% fall in ULVPV. PLVP was unchanged. Thus in DOCA-treated pigs, LVP appears not to be involved in the development of hypertension, but may be involved in its maintenance.
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PMID:Increased urinary vasopressin excretion in the DOCA-hypertensive pig. 636 64

Subcutaneous injections of elcatonin, a synthetic analogue of eel calcitonin, lowered the blood pressure in DOCA/saline-hypertensive and spontaneously hypertensive rats (SHR), but not in normotensive Wistar rats. The hypotensive effect was more prominent in the DOCA hypertensive rats. Daily injections of elcatonin (10-30 U/kg/day for 21 days) resulted in maximum hypotension on the 4th day in DOCA hypertensive rats and on the 14th day in SHR, and the reduced level of blood pressure was maintained. After the cessation of elcatonin injections, the pressure started to elevate gradually towards the control level. In normotensive rats, elcatonin did not significantly alter the blood pressure for 6 weeks. Daily injections of elcatonin significantly prevented the development of DOCA-induced hypertension and spontaneously-occurring hypertension. Elcatonin-induced hypotension did not differ in the control and parathyroidectomized DOCA hypertensive rats. Elcatonin did not alter the pressor response to noradrenaline, vasopressin and angiotensin II nor the depressor response to isoproterenol, acetylcholine and histamine in DOCA hypertensive rats. It is concluded that the antihypertensive effect of elcatonin is not associated with the release of parathyroid hormone nor with the blockade of alpha, beta, angiotensin II and vasopressin receptors.
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PMID:[Antihypertensive action of elcatonin]. 667 29

In conscious rats with near-malignant phases of DOCA-salt (DS) hypertension, hemodynamics were studied with microspheres before and after administration of a vasopressin (VP) vasopressor antagonist in relation to plasma VP levels (pVP). Compared to the controls, the DS rats showed significant elevations in mean arterial pressure (MAP), total vascular resistance (TVR), and pVP, and a flow redistribution from kidney and spleen to skeletal muscles and heart, with increased vascular resistance in almost all organs. The antagonist elicited no significant systemic hemodynamic effects in DS rats as a whole; however, two subgroups, responders vs nonresponders, were identified according to the effects on MAP. In responders with a pVP of 29.2 +/- 2.7 (SE) pg/ml, the antagonist lowered MAP (-24.9 +/- 5.9 mm Hg) and TVR significantly, while in nonresponders with a pVP of 15.2 +/- 3.4 pg/ml, there were no effects. The major antagonist-induced regional responses were increased flow and decreased vascular resistance in skeletal muscles and skin in whole DS rats, and additionally in the gastrointestinal tract, portal organs, and testes in the responders. Significant correlations were observed between pVP, MAP, TVR, and depressor responses to the antagonist only when all data for DS and control rats were pooled. Thus, the systemic hemodynamic effects of VP are important only in responders with exceedingly elevated pVP. VP contributes significantly to the regional hemodynamic abnormalities in skeletal muscles and skin in whole DS rats, and also in several other organs in the responders.
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PMID:Cardiovascular hemodynamics and vasopressin blockade in DOCA-salt hypertensive rats. 673 59

To determine the role of vasopressin in the maintenance of high blood pressure, the antihypertensive effect of the antagonists of the vasopressor effect of vasopressin, [1-deaminopenicillamine, 4-valine, 8-D-arginine] vasopressin (dPVDAVP), and [1-(beta-mercapto-beta, beta-cyclopentamethylenepropionic acid), 4-valine, 8-D-arginine] vasopressin (cyclo dVDAVP), was studied in unanesthetized, nonsurgically stressed rats with adrenal regeneration hypertension, malignant DOCA-salt hypertension, and malignant two-kidney, one clip Goldblatt hypertension. The doses of vasopressin antagonist used blocked the blood pressure (BP) response to vasopressin almost completely, with no changes in the pressor response to norepinephrine and angiotensin II. Administration of the vasopressin antagonists did not induce significant changes in the mean BP in any of the three experimental groups studied. It is suggested that in unanesthetized, nonsurgically stressed rats with adrenal regeneration hypertension, malignant DOCA-salt hypertension, and malignant two-kidney, one clip Goldblatt hypertension, vasopressin does not have a role in the maintenance of high BP.
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PMID:Evidence against a role of vasopressin in the maintenance of high blood pressure in mineralocorticoid and renovascular hypertension. 700 26

1. Arginine vasopressin was infused at 0.5, 2, 6, 18 or 54 ng min(-1) kg(-1) for 1 hr into normal, sham-operated and DOCA-salt hypertensive rats. Complete vasopressin/blood pressure dose-response curves were constructed from circulating plasma vasopressin concentrations measured at the end of each infusion. 2. DOCA-salt hypertensive rats had a higher basal plasma vasopressin concentration (11.1 +/- SD 3.7 fmol/ml) than either the normal (3.9 +/- 2.3, P less than 0.01) or the sham-operated rats (4.5 +/- 2.4, P less than 0.01). 3. The DOCA-salt hypertensive rats did not have my detectable enhancement of pressor sensitivity, compared with either of the two normotensive groups. 4. There was no significant increase in blood pressure in either the normal rats or sham-operated rats until vasopressin was infused at 2 ng min(-1) kg(1), when the plasma concentration was between 30 and 40 fmol/ml. 5. Subpressor infusion of vasopressin in the normal and sham-operated rats, which gave plasma concentrations of 22-23 fmol/ml, completely suppressed plasma angiotensin II to levels similar to the basal values found in the DOCA- salt hypertensive rats (10.5 +/- 2.3, 14.5 +/- 4.5 and 8.0 +/- 1.6 fmol/ml respectively). 6. These findings suggest that the mechanism of vasopressin involvement in DOCA-salt hypertension is as yet unclear, that short-term changes in vasopressin concentration appear unimportant in the regulation of normal blood pressure, that small physiological changes of vasopressin in normal rats may be important in the regulation of renin secretion, and that the increase in vasopressin concentration seen in DOCA-salt hypertension may contribute to the suppression of renin and angiotensin II in this state.
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PMID:Effect of acute vasopressin infusion on blood pressure and plasma angiotensin II in normotensive and DOCA-salt hypertensive rats. 705 14

To examine the role of vasopressin (VP) in DOCA-salt hypertension, arterial pressure and renal vascular reactivity were studied in control Long-Evans (LE) rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). Vascular reactivity to norepinephrine, VP and angiotensin II was assessed in isolated kidneys perfused at constant flow. LE rats showed an increase in arterial pressure (AP) which was significant at 2 weeks post DOCA and averaged 180 mm Hg at 4 weeks. DI rats lacking VP showed no rise in AP after DOCA; however, DI rats given VP and DOCA developed hypertension with a course and magnitude similar to that observed in LE rats. At 6 to 10 weeks post DOCA, renal vascular reactivity to all agents was increased in LE rats and DI rats replaced with VP. Normotensive DI rats lacking VP showed depressed reactivity. Assessment of changes in reactivity at 3 days post DOCA showed that changes preceded the rise in AP. These data suggest that VP may play a primary role in the pathogenesis of DOCA hypertension and that its mechanism may involve an induction of increased vascular reactivity.
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PMID:Vasopressin and vascular reactivity in the development of DOCA hypertension in rats with hereditary diabetes insipidus. 706 Nov 26

DOCA-salt hypertension does not develop in rats with hereditary lack of vasopressin (DI rats) nor in rats with lesion of the anteroventral region of the third ventricle (AV3V), an area controlling vasopressin (VP) release. We examined, therefore, the effect of VP treatment on the development of DOCA salt hypertension in AV3V-lesioned (AV3V-L) normal Sprague-Dawley rats and in Brattleboro rats homozygous for diabetes insipidus (DI rats). We also examined changes in vascular reactivity in isolated, perfused kidneys in the experimental groups. Whereas sham-lesioned (SL) rats showed hypertension at 5 weeks, AV3V-L rats showed no change in arterial pressure (AP) after DOCA. AV3V-L rats given VP exhibited only an intermediate rise in AP in spite of the fact that plasma VP levels were comparable in DOCA-treated SL rats and AV3V-L rats. SL and AV3V-L rats given VP showed enhanced renal vascular activity whereas no vascular changes occurred in AV3V-L rats. At 5 weeks post DOCA, intact DI rats given VP were hypertensive and exhibited enhanced renal vascular reactivity. AV3V lesion in DI rats completely prevented VP-induced DOCA/salt hypertension and enhanced vascular responsiveness. These data suggest that VP plays a primary role in DOCA-salt hypertension through an induction of enhanced vascular reactivity and through central mechanisms requiring the integrity of the AV3V region.
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PMID:Vasopressin-central nervous system interactions in the development of DOCA hypertension. 706 3

A 6-year-old girl developed generalized seizures followed by coma, five days after surgical removal of a craniopharyngioma. Low serum sodium levels and low serum osmolality with inappropriately high urinary sodium output confirmed the diagnosis of inappropriate antidiuretic hormone (ADH) secretion. Treatment with 3% hypertonic saline solution and repeated doses of furosemide (1 mg/kg) improved her clinical condition; serum sodium levels, however, rose slowly and urinary excretion remained high. Deoxycorticosterone acetate (DOCA), 4 mg/sq m/day, was added to the above regimen. A striking clinical improvement was noted. Serum sodium levels returned to normal with a concomitant sharp decline in urinary sodium output. The clinical course of this patient demonstrates the efficacy of the addition of deoxycorticosterone acetate to hypertonic saline and furosemide in the treatment of severe, life-threatening hyponatremia due to the syndrome of inappropriate antidiuretic hormone secretion.
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PMID:Combined treatment of severe hyponatremia due to inappropriate antidiuretic hormone secretion. 707 19


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