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

The decrease of sympathetic activity by the beta-blocking drug, as demonstrated by the decreased electric activity of the splanchnic nerve and by the decreased urinary catecholamine reponse to tilt as well as by the decreased levels of plasma dopamine beta-hydroxylase exists not only in hypertension with elevated PRA but also in hypertension with normal or low PRA. In these latter cases the antihypertensive effect is better explained by the decrease in the sympathetic nervous system activity than by the decrease of PRA. This effect seems to be indirect and probably, as suggested by Lewis, as a result of damping sensory input to the central nervous system from the heart, whose capacity to respond to exercice and stress is blunted by beta-adreno-receptor blockade.
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PMID:[The sympathetic nervous system inhibition in the antihypertensive effect of beta-blockers (author's transl)]. 2 20

Intact female Sprague-Dawley rats were given daily injections of either 3.125 mg of deoxycorticosterone or 5.0 mg of 16beta-hydroxy-dehydroepiandrosterone, calculated from the activities reported for each to be equivalent mineralocorticoid dosages. The former caused hypertension, cardiorenal enlargement, increased urine output and depressed PRA. Treatment with 16beta-OH-DHEA had no such effect, raising questions regarding its classification as a mineralocorticoid.
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PMID:Effect of deoxycorticosterone acetate and 16beta-hydroxy-dehydroepiandrosterone on blood pressure and plasma renin activity of rats. 13 67

The renin-angiotensin-aldosterone system has been evaluated in 19 patients with Cushing's syndrome due to bilateral adrenal hyperplasia and in 2 patients with unilateral adenoma. In the first group urinary aldosterone was within the normal limits with a mean of 8.3 +/- 1.86 microgram/24 h. Aldosterone excretion did not change significantly after furosemide administration, ACTH infusion or dexamethasone. Upright PRA was suppressed in 9/16 patients with a mean of 4.9 +/- 1.85 ng/ml/3 h and showed only a slight response to furosemide. Dexamethasone alone did not produce any change. Both aldosterone and PRA were to some extent stimulated by an association of dexamethasone and furosemide. In the 2 patients with adenoma, aldosterone excretion was also normal, but PRA was very elevated. From our data it is concluded that in Cushing's syndrome due to bilateral hyperplasia, PRA and aldosterone excretion are partially suppressed. From our results on plasma deoxycorticosterone and corticosterone concentration it seems unlikely that these mineralocorticoids are the major cause of this phenomenon. However, it may not be excluded that other yet unidentified hormones could play some role in the pathogenesis of hypertension and renin suppression in Cushing's syndrome.
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PMID:Plasma renin activity and urinary aldosterone in Cushing's syndrome. 20 67

A syndrome is described whose features, suggestive of primary mineralcorticoid excess, included hypertension, hypokalemia, low PRA, and responsiveness to spironolactone. Aldosterone levels were subnormal but as yet there has been no evidence of overproduction of other mineralocorticoids by chemical analysis or by bioassay of plasma and urinary extracts. The steroidal abnormalities that were observed involved peripheral matabolism rather than secretion. One patient exhibited a transient delay in reduction of the 3-keto group in the A ring, and both patients exhibited a decrease in the metabolism of cortisol to biologically inactive cortisone. This was shown by the marked decrease in the excretion of urinary metabolites bearing an 11-keto group and a decrease in the oxidation of 11 alpha-[3H]cortisol to tritiated water. The defect appeared not to be a deficiency of the 11 beta-oxidoreductase system itself, since the reverse reaction of conversion of cortisone to cortisol proceeded normally, but, rater, an alteration in the equilibrium position of 11 beta-oxidoreduction in favor of the reduced form. This was also expressed by a prolongation of the half-time of disappearance of cortisol. The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion. The decreased rate of conversion of cortisol to cortisone serves as a biochemical marker of this hypertensive syndrome.
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PMID:A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol. 22 61

Ten children with hypertension poorly controlled with other drugs and high peripheral plasma renin activity after renal transplantation were treated with propranolol. The mean systolic pressure decreased from 139 to 127 mm Hg (p less than 0.05) and the mean diastolic pressure from 98 to 83 mm Hg (p less than 0.01). Eight children had an antihypertensive response; two did not respond. The maximum dose of propranolol in responders varied from 1.0 to 6.2 mg/kg/day and duration of treatment until response varied from four to 49 days. PRA, repeated in seven responders, decreased in all (p less than 0.01). There was no correlation between changes in PRA and blood pressure. Propranolol was well tolerated and was a valuable antihypertensive drug in these children.
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PMID:Treatment of high-renin hypertension with propranolol in children after renal transplantation. 31 85

The antihypertensive effect of atenolol, with and without chlorthalidone, on hypertension was assessed in an outpatient as well as in an inpatient study. In the outpatient study atenolol alone induced decreases in systolic and diastolic BP amounting to 20 and 15 mm Hg. Maximal response of BP and HR developed within a week at the lowest dose used (100 mg twice daily). Combined atenolol-chlorthalidone treatment decreased lying and standing systolic BP by 7 and 14 mm Hg more than atenolol alone, but diastolic BP was decreased little more. In the inpatient study the addition of atenolol to chlorthalidone therapy in a dose of 100 mg twice daily resulted in a maximal decrease in BP within 3 days. At this dose PRA was lowered only slightly. Larger doses did not lead to any significant further decrease in BP, whereas PRA fell progressively. Our results indicate that, in contrast to nonselective blockade, specific beta-1-adrenoceptor blockade by atenolol is capable of inducing a distinct antihypertensive effect, unrelated to suppression of PRA. The decrease in PRA after larger doses of atenolol was not accompanied by a further decrease in BP. Because diuretic-induced renin release plays a role in the maintenance of the BP, our findings suggest that at higher dosages a hypertensive effect of the beta blocker compensated for the hypotensive effect of the decrease in PRA.
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PMID:Atenolol and chlorthalidone on blood pressure, heart rate, and plasma renin activity in hypertension. 36 78

13 patients (9 females, 4 males) with hypertension and unilateral (non-vascular) small kidney underwent nephrectomy. Before surgery, renin activity (PRA) was measured in renal vein blood before and/or 15 and 30 minutes after intravenous stimulation with 40 mg furosemide. From these PRA values renin rations (PRA affected side/PRA unaffected side) were calculated. A ratio of greater than or equal to 1.5 was considered to be significant. After a mean postoperative observation period of 3.9 +/- 1.3 years 6 patients (46%) were cured and 6 were improved. In only 1 patient (8%) did hypertension remain unchanged. No differences could be observed between the renin ratios of cured and improved cases. Furthermore, in no patient was a correlation found between preoperative renin ratios and the degree of postoperative blood pressure reduction. Finally, both patients with renin ratios less than or equal to 1.4 were cured by surgery. Marked differences between cured and improved patients were seen in preoperative blood pressure values, age, duration of hypertension and renal function. Cured patients were younger and had much lower mean systolic and diastolic blood pressure values, shorter duration of hypertension and better renal function than improved patients. These results show that the diagnostic and prognostic validity of renal venous renin ratios is very limited in patients with a unilateral (non-vascular) small kidney. In these patients the effect of nephrectomy can already be predicted by analyzing simple anamnestic, clinical and chemical data.
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PMID:[Hypertension in unilateral (non-vascular) nephrosclerosis: renin activity in the venous kidney blood and effect of nephrectomy]. 39 19

The renin-angiotensin-aldosterone system in patients with acromegaly was evaluated by infusing [sarcosine1, isoleucine8]angiotensin II, a competitive angiotensin II antagonist, into five acromegalic patients with hypertension and three normotensive acromegalics. The drug was infused at a rate of 600 ng/kg . min for 30 min, 1 h after iv injection of 40 mg furosemide. In addition, before the infusion, plasma samples were obtained for determination of PRA and plasma aldosterone concentration. A significant pressor response to [sarcosine1, isoleucine8]angiotensin II was observed in all eight patients. Preinfusion PRA and plasma aldosterone concentration were significantly lower than in normal controls. It is concluded that in acromegaly, the renin-angiotensin-aldosterone system is suppressed and that this system is probably not involved in maintenance of the high blood pressure observed in some acromegalic patients.
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PMID:Blood pressure response to an angiotensin II antagonist in patients with acromegaly. 42 97

We studied 29 normotensive men (14 black, 15 white) and 36 hypertensive men (27 white, nine black) to examine the association of race with blood pressure, blood volume, and peripheral renin activity (pra). Blood volume was lower in white hypertensive men than in white normotensive men, but was similar in all blacks. When subjects were tested in the supine position, PRA was lower in black normotensive subjects than white normotensive subjects. The PRA did not differ among groups tested in an upright posture, while furosemide-stimulated PRA was lower in hypertensive than normotensive subjects of both races despite lower blood volumes in white hypertensive subjects. Differences of volume and renin measurements appear to reflect basic differences between whites and blacks with essential hypertension. We emphasize the need to consider race in the investigation of human hypertension.
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PMID:Racial analysis of the volume-renin relationship in human hypertension. 43 69

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.
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PMID:Plasma renin activity and urinary aldosterone in acromegaly. 48 12


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