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

Abnormalities in the hypothalamo-pituitary-adrenal axis in spontaneously hypertensive rats (SHR) during development of hypertension were investigated using in vivo and in vitro methods. Plasma ACTH responses to hemorrhage and ether stress were significantly smaller in 7-week-old SHR than in age-matched Wistar-Kyoto rats (WKY), while plasma corticosterone baseline levels and its response to stress were greater in SHR than in WKY. There was no significant difference in the plasma ACTH response to ether stress between bilaterally adrenalectomized SHR and WKY replaced with a 25% corticosterone pellet for 6 days. Adrenalectomy prevented the development of hypertension in SHR; however, corticosterone replacement restored hypertension. Plasma ACTH showed a smaller response to iv CRH injection in SHR than in WKY, while the ACTH response to arginine vasopressin was not different between SHR and WKY. CRH concentrations in the median eminence, posterior pituitary, and cerebral cortex were lower in SHR than in WKY, while the CRH concentration in the median eminence was not different in SHR and WKY when they were adrenalectomized with or without corticosterone replacement. Basal in vitro CRH release from hypothalamic tissue was reduced in SHR, while CRH release in response to 56 mM KCl was not different in SHR and WKY. These results suggest that adrenocortical function is enhanced in young SHR, that reduced ACTH response to stress and exogenous CRH in SHR may be ascribed to higher plasma corticosterone levels, and that corticosterone is essential for the development of hypertension in SHR.
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PMID:Abnormalities in the hypothalamo-pituitary-adrenal axis in spontaneously hypertensive rats during development of hypertension. 254 78

We studied the hormonal background of the fluid derangements and arterial hypertension associated with adrenocorticotrophic hormone (ACTH) treatment for infantile spasms in ten infants aged 5-22 months. They received a 6 week course of (carboxymethyl-cellulose-)ACTH: 80 IU at 0800 hours daily in weeks 1-3, then tapering, and termination at the end of week 6. The infants showed large, variable increases in 24 h urine cortisol during treatment. The mean plasma cortisol concentration (24 h after ACTH injection) was not significantly increased, but was correlated with the relative dose of ACTH. The mean plasma aldosterone concentration decreased. No significant change occurred in plasma renin activity (PRA), or in the concentrations of renin substrate (RS) or arginine vasopressin (AVP). Seven infants developed arterial hypertension, which was severe in three. This severe hypertension was associated with the highest relative ACTH doses and the highest plasma RS and cortisol concentrations. In the group as a whole, systolic blood pressure correlated with plasma RS and cortisol concentrations, but not with the other parameters. At the end of treatment urine and plasma cortisol dropped below the pretreatment levels and stayed low for greater than 2 weeks. There was a sharp peak in PRA and plasma aldosterone concentration, and a decrease in plasma RS. Plasma AVP levels dropped markedly. The mean body weight increased sharply and urine flow decreased. Mean plasma electrolyte levels remained unaltered. The danger at termination of ACTH treatment appears to be associated with a sudden transition from hypercortisolism to hypocortisolism, activation of the renin-angiotensin-aldosterone axis, and suppression of AVP secretion.
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PMID:Hormonal background of the hypertension and fluid derangements associated with adrenocorticotrophic hormone treatment of infants. 255 92

The natriuretic effects of atrial peptide hormones have been attributed, at least in part, to their stimulation of guanylate cyclase activity in renal cell membranes. The effects of atrial natriuretic factor (ANF) on stimulation of cyclic guanosine monophosphate (cGMP) and cyclic adenosine monophosphate (cAMP) accumulation were investigated in cloned human kidney tumor (hKT) cells and parent cells from a human renal tumor epithelial cell line (SK-NEP-1). Human ANF-(99-126) (10(-6)M) stimulated (p less than 0.001) cellular cGMP accumulation in a dose-dependent manner from a basal level of 0.26 +/- 0.04 to 3.73 +/- 0.81 pmol/mg protein/5 mi (mean +/- SEM, n = 13). ANF stimulation of cGMP accumulation was specific, in that high concentrations (10(-6)M) of atriopeptin I [rat ANF-(103-123)], angiotensin II, arginine vasopressin, and amiloride (10(-4)M) did not increase basal cGMP. Amiloride (10(-4)M) enhanced (p less than 0.01, n = 6) the ANF stimulation of cGMP accumulation (1.24 +/- 0.39 pmol/mg protein/5 min), particularly at low doses of ANF (10(-10)M) where stimulation by ANF without amiloride (0.34 +/- 0.08 pmol/mg protein/5 min) was barely distinguishable from a basal level (0.19 +/- 0.02 pmol/mg protein/5 min) of cGMP accumulation. The stimulatory effect of ANF (1.59 +/- 0.07 pmol/mg protein/5 min) was attenuated (0.75 +/- 0.06 pmol/mg protein/5 min, p less than 0.01, n = 6) by preincubation of the cells with pertussis toxin but not by cholera toxin. ANF (4.56 +/- 0.93 pmol/mg protein/5 min, n = 8) did not affect cAMP accumulation (4.32 +/- 0.98 pmol/mg protein/5 min) in hKT cells. This is the first report of an ANF responsive human renal cell line, and its use should facilitate investigation of ANF-receptor interactions.
Hypertension 1989 Jun
PMID:Atrial natriuretic factor effects on cyclic nucleotides in a human renal cell line. 256 5

It has been hypothesized that moderately increased blood levels of arginine vasopressin (AVP) contribute to the development and/or maintenance of hypertension. In this study, male Sprague-Dawley rats on a fixed 1 meq daily sodium intake received 10-day intravenous infusions of 0.2 and 2.0 ng.kg-1.min-1 AVP. The higher infusion rate was above the acute vasoconstrictor threshold for AVP administration and also produced a maximal antidiuretic effect. During chronic AVP administration, however, daily mean arterial pressure, heart rate, and body fluid composition were not changed, despite a maintained antidiuresis. To test the hypothesis that circulating AVP failed to cause hypertension as a result of sensitization of the baroreflex or a direct sympathoinhibitory effect of the peptide, additional experiments were performed in rats subjected to sinoaortic denervation (SAD) or ablation of the area postrema (APX). Infusion of AVP for 10 days into SAD or APX rats caused a sustained antidiuresis but did not change arterial pressure, heart rate, or body fluid composition. In all groups of rats, the depressor response to ganglionic blockade (20 mg/kg hexamethonium) was used to estimate the autonomic component of resting arterial pressure; no change in autonomic cardiovascular control was found using this method in any of the groups during AVP infusion. Long-term elevation of plasma AVP in rats, therefore, does not cause hypertension or significantly affect autonomic regulation of arterial pressure.
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PMID:Effect of circulating vasopressin on arterial pressure regulation in rats. 256 56

To determine whether the effects of arginine vasopressin (AVP) on the renal and systemic vessels are modulated by prostaglandins (PGs), AVP (10, 20, and 50 mU/kg/min) was infused into the renal artery before and after treatment with indomethacin (8 mg/kg) in anesthetized rabbits. Arginine vasopressin elicited a dose-dependent increase in systemic arterial pressure and renal vasoconstriction. However, after cessation of the infusion, significant renal vasodilation was observed. Indomethacin potentiated the systemic and renal vasoconstrictor actions and attenuated the renal vasodilator reaction induced by AVP. These results suggest that endogenously produced PGs buffer the vasoconstrictor action of AVP, and the renal vasodilator reaction induced by AVP could be mediated through PGs. Further, to investigate whether the effects of AVP on the systemic and renal vessels are mediated by calcium ion (Ca++), the Ca++ entry blocker nifedipine was used. Intravenous administration of nifedipine (50 micrograms/kg) attenuated the systemic and renal vasoconstrictor action of AVP. The renal vasodilator reaction induced by AVP was also diminished after treatment with nifedipine. These results indicate that the systemic and renal vasoconstrictor actions of AVP are mediated through Ca++ influx into the vascular smooth muscle cells. The present study suggests that Ca++ participates in the AVP-induced vasodilator reaction, itself probably mediated by PGs.
Hypertension
PMID:Interaction of vasopressin and prostaglandins through calcium ion in the renal circulation. 257 5

The role of vasopressin (AVP) and angiotensin II (ANG II) in the onset of acute (45 min) aortic coarctation hypertension was studied in conscious rats. Changes in mean carotid pressure (MCP) and heart rate (HR) were measured in four groups of rats. Control rats presented a hypertensive response that attained a plateau 5 min after coarctation and remained near this level throughout the experiment. Rats treated with AVP V1-vascular receptor antagonist [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine]arginine vasopressin [d(CH2)5Tyr(Me)AVP] presented a prompt rise in MCP similar to the control rats, but in contrast to this group, the MCP started to decline progressively. Rats treated with saralasin presented a delay in the onset of hypertension right after coarctation but slowly attained values similar to those for control rats. In contrast, the rats treated with AVP antagonist plus saralasin showed a blunted MCP elevation throughout the experiment. Reflex bradycardia observed in the rats treated with saralasin or the AVP antagonist plus saralasin was similar to that observed in the control rats, whereas for the group treated only with AVP antagonist, the reflex bradycardia was more intense than for the other three groups, indicating an increased sensitivity of the baroreflex. These data demonstrate that in addition to the mechanical effect of aortic constriction, both ANG II and AVP participate in the onset of acute aortic coarctation hypertension. Moreover, the results indicate that ANG II acts on the prompt (5 min) rise in pressure, whereas AVP is responsible for the maintenance (30-45 min) of the arterial pressure elevation.
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PMID:Acute aortic coarctation hypertension: role of vasopressin and angiotensin II. 258 3

Epidemiologic studies suggest an inverse relation between potassium intake and the prevalence of hypertension. To investigate the effect of dietary potassium restriction on blood pressure, we used a randomized crossover design to study 10 healthy, normotensive men randomly assigned to isocaloric diets (each lasting nine days) providing either low (10 mmol per day) or normal (90 mmol per day) amounts of potassium, while sodium intake was maintained at the subjects' usual levels (120 to 200 mmol per day). With the low-potassium diet, plasma potassium levels declined from 3.8 to 3.2 mmol per liter (P less than 0.001), but plasma sodium and chloride levels were unchanged. The average daily excretion of urinary sodium (+/- SEM) on the low-potassium diet was significantly lower than that with the normal-potassium diet (10 +/- 10 vs. 144 +/- 10 mmol; P less than 0.001). The mean arterial pressure did not change significantly during normal potassium intake, but it increased over the nine days of the low-potassium diet from 90.9 +/- 2.2 to 95.0 +/- 2.2 mm Hg (P less than 0.05). Both mean arterial (P less than 0.01) and diastolic (P less than 0.005) pressures were significantly higher after the low-potassium diet than after the normal-potassium diet. Potassium depletion suppressed plasma aldosterone levels but had no effect on plasma renin activity or on arginine vasopressin or catecholamine levels. A saline infusion further increased the mean arterial pressure in the potassium-depleted subjects but had no effect in the control group (P less than 0.05). We conclude that short-term potassium depletion increases blood pressure in healthy, normotensive men and permits further increases in blood pressure after saline loading. We found no evidence that the hypertensive effect of potassium depletion resulted from changes in either renal hemodynamics or circulating levels of vasoactive hormones.
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PMID:Increased blood pressure during potassium depletion in normotensive men. 281 51

The role of vasopressin in the regulation of body water volume and its distribution to intravascular, interstitial and intracellular compartments, and the importance of particular body water compartments in the pathogenesis of DOCA-salt hypertension were studied in young Brattleboro rats. Vasopressin-deficient, vasopressin-synthesizing and vasopressin-deficient rats chronically supplemented with deamino-8-D-arginine vasopressin (dDAVP) were compared with water-drinking controls. The chronic DOCA-salt treatment caused a marked hypertension in vasopressin-synthesizing animals; in these animals body water was slightly increased due to the expansion of extra-cellular fluid volume whereas intracellular water tended to decrease, so that the ratio of extracellular fluid volume to intracellular water rose significantly. The development of DOCA-salt hypertension was attenuated in the vasopressin-deficient rats, which had a similar level of total body water, slightly increased intracellular water and significantly decreased extracellular fluid volume compared with the hypertensive vasopressin-synthesizing rats. Consequently, in the vasopressin-deficient rats, the ratio of extracellular fluid volume to intracellular water did not differ from that of controls. A vasopressin deficiency was associated with a failure to expand the interstitial fluid volume although plasma volume was increased. Unaltered total body water together with elevated plasma osmolality indicated an extracellular water deficiency in DOCA-salt-treated vasopressin-deficient rats. Chronic dDAVP supplementation restored the body fluid pattern and the hypertensive response of the DOCA-salt-treated vasopressin-deficient rats. In conclusion, the antidiuretic effects of vasopressin are necessary for the interstitial fluid volume expansion that is essential for a full development of DOCA-salt hypertension.
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PMID:Vasopressin and water distribution in rats with DOCA-salt hypertension. 263 18

Twenty-four adults who were undergoing operations on the abdominal aorta were enrolled in a randomized, double-blind, placebo-controlled study in which epidural morphine sulfate (6 mg) was employed to attenuate the sympathoadrenal response to surgery to evaluate the possible contribution of sympathetic nervous system hyperactivity to postoperative hypertension. Patients who received epidural morphine required less parenteral morphine in the 24 hours following surgery, had lower analogue pain scores, and had markedly lower plasma norepinephrine levels when compared with patients in the control group who received an identical volume of saline in the epidural space. Epidural morphine had no effect on plasma epinephrine or arginine vasopressin levels. Fewer patients in the morphine group (4 of 12 vs 9 of 12 patients in the saline group) required treatment for hypertension (mean arterial blood pressure, greater than or equal to 110 mm Hg) in the 24 hours following surgery. In addition, patients in the morphine group had lower blood pressures in the 24 hours following surgery. These data suggest that sympathetic nervous system activity and not adrenal epinephrine or pituitary secretion of arginine vasopressin is responsible for the development of hypertension following aortic surgery. Furthermore, epidural narcotics appear to provide a means of attenuating this response.
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PMID:Epidural morphine decreases postoperative hypertension by attenuating sympathetic nervous system hyperactivity. 272 4

The effect of arginine vasopressin (AVP) on the arterial baroreflex control of heart rate (HR) was studied in intact and sinoaortic-denervated (SAD) conscious, unrestrained monkeys. A baroreflex curve for mean arterial blood pressure (MABP) and HR was determined before and during intravenous infusion of AVP (2-4 mU.kg-1.min-1) and after the AVP vascular antagonist "Manning compound" [( d(CH2)5Tyr(Me)]AVP, 40 micrograms/kg), while AVP infusion was kept running. The sensitivity (slope) of the arterial baroreflex, as well as the reflex bradycardia induced by high blood pressure, increased significantly during AVP and returned to the control level after Manning compound. The effect of AVP on the Bezold-Jarisch reflex (induced by stimulating left ventricular receptors with 4 micrograms/kg veratridine injected in the left atrium) was also studied. The cardiovascular responses to veratridine were examined before and during AVP and after administration of Manning compound together with AVP infusion. AVP significantly potentiated the hypotension and the bradycardia produced by veratridine, whereas Manning compound blunted this potentiation. The ventricular reflex in SAD monkeys was significantly greater than in intact monkeys. We conclude that, in the conscious nonhuman primate, AVP potentiates the sensitivity of the baroreflex control of HR as well as the Bezold-Jarisch reflex. The potentiation of the Bezold-Jarisch reflex by AVP in the SAD animals is consistent with a central action, since the baroreceptors and ventricular receptors both have connections in the nucleus tractus solitarius. However, it does not rule out the possibility of peripheral actions on receptors or end organs.
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PMID:Vasopressin potentiates ventricular and arterial reflexes in the conscious nonhuman primate. 273 28


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