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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One-kidney, figure-8 renal wrapped and sham-operated rats maintained on high sodium intake were studied to determine plasma concentrations of vasopressin during the onset of hypertension. Animals were chronically prepared with femoral artery and vein catheters. Arterial blood samples were taken from conscious rats before and 3 days after renal wrap or sham operation while donor blood was simultaneously infused intravenously. Three days after surgery, arterial pressure, plasma osmolality and plasma vasopressin concentration increased significantly in the renal wrapped animals and remained unchanged in the sham-operated rats. Ganglionic blockade with hexamethonium and atropine produced equivalent decreases in arterial pressure and increases in plasma vasopressin concentration in the two groups of rats. Subsequent administration of the V1 vasopressin antagonist, d(CH2)5Tyr(Me)AVP, caused a significantly greater fall in arterial pressure in the hypertensive rats. These results provide further evidence for a contribution of vasopressin to sodium-dependent hypertension.
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PMID:Plasma vasopressin concentration in high sodium renal hypertension. 379 28

The role of vasopressin (VP) in maintaining blood pressure in malignant two-kidney one-clip Goldblatt hypertension in chronically catheterized conscious rats was investigated by studying the effect of two structurally different VP pressor antagonists. Injections of either 20 micrograms/kg of dPTyr(Me)AVP or 10 micrograms/kg of d(CH2)5Tyr(Me)AVP failed to alter mean arterial pressure or heart rate, although both antagonists completely inhibited the pressor response elicited by exogenous VP. These results suggest, that VP is not involved as a pressor hormone in the maintenance of high blood pressure in this type of experimental hypertension.
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PMID:Effect of vasopressin blockade on blood pressure in conscious rats with malignant two-kidney Goldblatt hypertension. 384 65

To investigate the possible role of vasopressin (VP) in the maintenance of DOC-salt hypertension the effect of two VP pressor antagonists on mean arterial pressure and the pressor responsiveness to exogenous VP were studied in conscious, freely moving rats with malignant DOC-salt hypertension. Intravenous injections of either 20 micrograms/kg of dP Tyr(Me)AVP or 10 micrograms/kg of d(CH2)5Tyr(Me)AVP had no significant effect on mean arterial pressure and heart rate, although both antagonists almost completely abolished the pressor response to VP. Furthermore, the animals with DOC-salt hypertension exhibited decreased pressor responsiveness to exogenous VP. The present findings strongly suggest that VP is not essential as a pressor hormone for maintaining blood pressure in malignant DOC-salt hypertension.
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PMID:Evidence against a vasopressor role of ADH in malignant DOC-salt hypertension. 384 Oct 34

Systemic administration of the GABA antagonist picrotoxin 6.0 mg/kg i.v. elicited hypertension and a fall in sinus rate with a return to baseline levels in intact rats. Antagonists of GABA act in the supraspinal CNS to augment sympathetic outflow to the heart and vasculature. Therefore, in this study the spinal cord was transected prior to drug administration in order to eliminate sympathetically mediated effects. In spinal rats, picrotoxin 6.0 mg/kg evoked a biphasic sinus rate response characterized by an initial decrease followed by an increase above baseline sinus rate. Bilateral vagotomy or atropine pretreatment blocked sinus rate changes elicited by picrotoxin, demonstrating that these effects were vagally mediated. Midcollicular decerebration altered the biphasic sinus rate response by preventing the late rise but not the initial decrease in sinus rate. Infusion of another GABA antagonist, bicuculline, elicited a similar biphasic sinus rate response, although the time-course was shorter. Unexpectedly, picrotoxin or bicuculline administration in spinal rats caused an increase in mean blood pressure which was prevented by decerebration and different from that observed in intact rats with respect to time course. In spinal rats pretreatment with a vasopressin antagonist, D(CH2)5Tyr(Me)AVP, blocked the pressor response induced by picrotoxin infusion without altering the biphasic changes in sinus rate. These results suggest that, in the rat: (1) two GABAergic inhibitory mechanisms at different levels of the neuraxis exert opposite effects on cardiac vagal activity; and (2) GABA antagonists may elevate arterial pressure by a mechanism distinct from their previously described sympathoexcitatory effects.
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PMID:Biphasic effects of systemically administered GABA antagonists on cardiac vagal activity. 394 99

In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increases in blood pressure and left ventricular weight with typical histological changes in the kidney. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 +/- 0.5 to 8.9 +/- 0.8 pmol/l) but significantly more in SHR (from 5.0 +/- 0.6 to 15.8 +/- 1.2 pmol/l). Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10 micrograms/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 +/- 0.9 mmHg (P less than 0.05) and 9.7 +/- 1.7 mmHg (P less than 0.05) respectively. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 +/- 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggests a close relationship between plasma AVP and severity of hypertension. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.
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PMID:Contribution of vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats. 395 9

Biochemical, cytochemical and immunological methods were used to compare the metabolic and neuroendocrine properties of the subfornical organ (SFO) with the hypothalamo-neurohypophysial system (HNS) in the rat. The SFO resembles the HNS in that both have (a) increased label incorporation into RNA during dehydration; (b) an intense reaction for glucose-6-phosphate dehydrogenase; (c) NADPH-diaphorase and the Type I pathway for hydrogen utilization from NADPH, presumably as part of the mixed-function oxidase system for the metabolism of endogenous substrates and xenobiotics; (d) immunoreactive vasopressin and oxytocin. Gel filtration of extracts of the SFO area using Sephadex G-25 chromatography resulted in immunoreactive peaks for both AVP and OT which were similar to synthetic hormones. One other fraction in the SFO extract, containing a substance(s) of higher molecular weight than AVP, was detected using the antiserum for AVP. The concentration of immunoreactive AVP in the SFO area was increased after colchicine, decreased by hypophysectomy, and unaltered by: (a) infusion (4.6 pg/min for 3 hr) or injection (1 or 6 ng) of AVP into the lateral cerebroventricle; (b) dehydration; (c) renin administered intracerebroventricularly; (d) pinealectomy; or (e) hypertension in the spontaneously hypertensive rat. In conclusion, cells in the SFO have specialized metabolic and neuroendocrine properties similar to the HNS. It can be inferred from these biochemical specializations that the SFO has metabolic and secretory activities.
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PMID:The subfornical organ: biochemical and neuroendocrine comparisons with the hypothalamo-neurohypophysial system. 402 8

Renal plasma flow, glomerular filtration rate plasma angiotensin II, aldosterone and arginine vasopressin, free water clearance, blood pressure and body weight in 11 patients with mild to moderate hypertension were determined at the end of consecutive 6 week periods of administration of placebo and verapamil up to 120 mg t.i.d. Verapamil induced a 10% reduction in diastolic blood pressure. Compared with placebo none of the other parameters measured changed after treatment with verapamil. There was no significant correlation between blood pressure and arginine vasopressin in plasma. It is concluded that verapamil reduced blood pressure by vasodilatation without activation of the counterbalancing mechanisms commonly seen after treatment with vasodilating drugs, i.e. tachycardia, activation of the renin-angiotensin-aldosterone system, water and salt retention, and without affecting renal haemodynamics. AVP does not seem to be involved in blood pressure regulation in mild to moderate essential hypertension.
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PMID:Effect of verapamil on renal plasma flow, glomerular filtration rate and plasma angiotensin II, aldosterone and arginine vasopressin in essential hypertension. 407 25

1. Blood pressure, heart rate and cardiac output were studies in intace conscious sheep during AVP infusion at 0.1, 0.25, 0.5 and 1.0 microgram/min for 30 minutes to determine whether pressor responsiveness to AVP was altered in ACTH-induced hypertension. 2. Prior to ACTH treatment, AVP produced rises in blood pressure associated with a fall in heart rate and cardiac output. 3. During ACTH treatment, pressor responsiveness to AVP and decrease in cardiac output were unchanged, but reflex bradycardia was reduced. 4. ACTH-induced hypertension in sheep is not associated with enhanced pressor responsiveness to AVP.
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PMID:Effect of ACTH administration on the haemodynamic response to arginine-vasopressin in sheep. 625 6

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

Alcoholics during detoxification have elevated blood pressures which are related to the severity of their withdrawal symptoms. We studied the effect of a non-selective beta-blocker, timolol on symptoms, blood pressure and plasma levels of cortisol (PC), noradrenaline (NA), vasopressin (AVP) and renin activity (PRA) during alcohol withdrawal. Eighteen alcoholics, admitted for detoxification, were randomly allocated to timolol or placebo in a double blind trial. Alcohol withdrawal symptoms did not differ either before or after timolol or placebo but patients receiving timolol required less sedation with chlormethiazole. Systolic blood pressures (SBP) and pulse both fell significantly during detoxification in both groups, the change being greater with timolol. Plasma levels of cortisol, NA, AVP and PRA fell significantly, though only NA and PC correlated with initial SBP. Timolol had no effect on any of the biochemical parameters observed. The pressor response to alcohol withdrawal is reduced by beta-blockade and the height of the blood pressure is related to plasma NA and PC levels. Alcohol withdrawal hypertension is probably due to increased sympathetic activity.
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PMID:The effect of a non-selective lipophilic beta-blocker on the blood pressure and noradrenaline, vasopressin, cortisol and renin release during alcohol withdrawal. 637 39


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