Effect of an Adrenal Inhibitor in Hypertensive Patients With Suppressed Renin

Woods, James W.

doi:10.1001/archinte.1969.00300140012004

Cited by 174 publications

(22 citation statements)

References 14 publications

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“…Approximately 25% of patients with essential hypertension have suppressed renin activity (14,(22)(23)(24)(25), and some investigators have suggested that these patients are volume-expanded (22,26,27). Since increased secretion of aldosterone is found in only a small fraction of these patients, secretion of other mineralocorticoid-like steroids has been assessed.…”

Section: Discussionmentioning

confidence: 99%

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Williams¹,

Braley²,

Underwood³

1976

J. Clin. Invest.

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A B S T R A C T 18-hydroxy 11-deoxycorticosterone (18-OH DOC), a weak mineralocorticoid, was estimated by a radioimmunoassay procedure after purification in 49 patients with hyper,tension and 38 normal control subjects. The sensitivity of the method was 2-4 pg; there was no detectable blank, and the precision was 9-10%. In normal subjects the absolute plasma levels were similar to those of aldosterone. ACTH administration produced a 23-fold increase, and sodium restriction resulted in a 4-fold increase (5.4+-0.7-20.5±3.0 ng/dl). On the other hand, the plasma levels of 18-OH DOC declined by nearly 50% with upright posture or angiotensin II infusion. During both of these procedures, plasma aldosterone levels significantly increased. Patients with normal and low renin hypertension had similar changes in plasma 18-OH DOC levels with sodium restriction. However, the mean high sodium level in the normal renin essential hypertension group (11.6±-1.6 ng/dl) was significantly greater (P < 0.001) than in the control group (5.4±0.7 ng/dl). In addition, at least 22% and perhaps as high as 37% of the hypertensive subjects had levels greater than the upper limits of normal on a high sodium intake. Differences between the groups were less impressive in the sodiumrestricted studies. There were no significant differences in age, duration of hypertension, sodium balance, serum sodium, potassium, or blood urea nitrogen in those patients who had elevated levels of plasma 18-OH DOC. Patients with primary aldosteronism had levels within -the normal range on both dietary intake. However, in contrast to the other groups there were no significant changes in the plasma levels with sodium restriction. Thus, a significant number of patients with essential hypertension presumably have an alteration in 18-OH DOC secretion.

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Section: Discussionmentioning

confidence: 99%

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Williams¹,

Braley²,

Underwood³

1976

J. Clin. Invest.

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“…Most patients with low-renin essential hypertension have normal secretion rates and urinary excretion rates of aldosterone, despite low plasma renin activity (1)(2)(3)(4). The secretion rate, exeretioni rate, and plasma levels of aldosterone do not suppress normally in response to sodium loading in patients with essential hypertension, particularly those with low plasma renin activity (5)(6)(7).…”

Section: Introductionmentioning

confidence: 99%

Increased Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

Wisgerhof¹

1978

J. Clin. Invest.

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A B S T R A C T Studies were undertaken to determine if the dissociation of aldosterone and plasma renin activity in low-renin essential hypertension is due to altered adrenal responsiveness to angiotensin II. The responsiveness of' the adrenal glands to angiotensin II was determined by infusing graded doses of angiotensin II into normal subjects and into patients with essential hypertension and measuring changes in levels of' plasma aldosterone in response to the infusion. To minimize the influence of endogenous angiotensin II and ACTH, supplemental sodium and dexamethasone were given before the infusions. Levels of plasma aldosterone and plasma renin activity were determined in normal subjects anid in the same patients after the combined stimuli of furosemide and upright posture, a maneuver used to increase the level of endogenous angiotensin II. To determine if the changes in levels of plasma aldosterone during infusion of angiotensin II were due to alteration of the metabolic clearance of aldosterone, the metabolic clearance of aldosterone was meastured before and during the infusion of angiotensin II.After sodium loading, dexamethasone treatment, and supine posture, levels of plasma aldosterone of normal subjects and patients with essential hypertension were suppressed equally. In response to the infusion of angiotensin II, the levels of plasma aldosterone of patients with low-renin essential hypertension were significantly higher than those of normal subjects or of patients with normal-renin essential hypertension.

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“…It now appears possible that the cellular defect of calcium handling is caused primarily by a derangement in transmembranous sodium transport. 1 In support of such a mechanism is the recent observation that calcium channel blockers, which inhibit the flux of extracellular calcium ions across the cell membrane, have the greatest antihypertensive effect in patients with low plasma renin levels' 4 -that is, in patients who presumably have an excess of total body sodium 15 as well as an intracellular sodium accumulation. 16 In the present study the short-term blood pressure and heart rate effects of verapamil were investigated in rats with hypertension induced by clipping one renal artery and removing the contralateral kidney.…”

Section: Discussionmentioning

confidence: 99%

Does renin determine the blood pressure response to calcium entry blockers?

Waeber

Nussberger²,

Brunner

1985

Hypertension

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SUMMARY Male Wistar rats with one-kidney, one clip renal hypertension were maintained on either a regular or a low salt diet for 3 weeks after clipping. At that time mean blood pressure in the unanesthetized rats was equally elevated in sodium-depleted (n = 17) and in sodium-replete rats (n = 19), but plasma renin activity was significantly higher in the former (p < 0.05). Infusion of the calcium entry blocker verapamll at a rate of 0.05 mg/kg/minute decreased blood pressure within 60 minutes to a similar extent in rats kept on a salt-deficient diet and in rats fed a regular salt diet. In all rats taken as a group, there was a close, direct correlation (r = 0.87, p < 0.001) between the magnitude of the blood pressure response to verapamil and the pretreatment blood pressure levels. Verapamil markedly accelerated heart rate and stimulated renin release in all rats. In additional groups of sodium-depleted (ii = 8) and sodium-replete renal hypertensive rats (n = 7), nifedipine administration (4 /xg/kg/min i.v.) within a 45-minute observation period caused a blood pressure fall (p < 0.001) and heart rate acceleration (p < 0.001) that were comparable in both groups. These findings suggest that in the rat with renal hypertension the short-term blood pressure response to the calcium antagonists verapamil and nifedipine is not influenced by the state of sodium balance and plasma renin activity. In this experimental model of hypertension, the magnitude of the blood pressure lowering effect of calcium entry blockers appears to be proportional to pretreatment blood pressure levels. (Hypertension 7: 223-227, 1985) KEY WORDS • renal hypertension high and low renin levels verapamil • nifedipine * conscious rats D URING recent years numerous studies have focused on the crucial role of intracellular free calcium in determining vascular smooth muscle tone.1 -2 Calcium channel blocking agents have been used to reduce intracellular calcium in an attempt to lower the blood pressure of hypertensive patients. Such drugs have proved to be helpful in managing hypertensive patients and appear particularly effective in reducing blood pressure when the rate of renin secretion is low.3 -4The present investigation was undertaken in conscious hypertensive rats to assess the effect of a change in sodium balance and renin release on the short-term blood pressure response to the calcium entry blockers verapamil and nifedipine. 5 The experiments were car- ried out in rats with hypertension induced by partially occluding one renal artery with the contralateral kidney removed (one-kidney, one clip renal hypertension) maintained postoperatively for 3 weeks on either a saltdeficient or a regular salt intake. As was known from previous work, 6 -7 blood pressure during the phase of established hypertension achieves similar high levels in sodium-depleted and sodium-replete rats in spite of the fact that plasma renin activity is elevated only in the former. Materials and MethodsMale Wistar rats weighing 140 to 180 g (Madorin AG, Fiillinsdorf, Switze...

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Effect of an Adrenal Inhibitor in Hypertensive Patients With Suppressed Renin

Cited by 174 publications

References 14 publications

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

The regulation of plasma 18-hydroxy 11-deoxycorticosterone in man.

Increased Adrenal Sensitivity to Angiotensin II in Low-Renin Essential Hypertension

Does renin determine the blood pressure response to calcium entry blockers?

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