Key result
Low-renin hypertensive patients showed aldosterone responses to physiological stimulations similar to normal-renin patients (3-5 fold increases), indicating multiple underlying mechanisms.
Why the study?
What are the mechanisms of aldosterone and renin suppression in low-renin hypertension?
Observational (n=67)
What are the mechanisms of aldosterone and renin suppression in low-renin hypertension?
Low-renin hypertension appears to be a heterogeneous clinical entity caused by various mechanisms rather than a single unknown mineralocorticoid.
Supports mechanistic heterogeneity in low-renin hypertension; leaves open whether this informs targeted therapies beyond current approaches.
Plasma renin activity and aldosterone were measured simultaneously in 67 out-patients with essential hypertension. High aldosterone was more often in patients with high renin, and low levels of aldosterone were usual in those with low and normal renin. In order to study the mechanism by which aldosterone and renin acitvity are suppressed in low-renin hypertension, 25 patients (13 normal-renin hypertensives, 10 low-renin patients including 4 non-responders and two DOC excess hypertensives) were investigated as inpatients. Plasma renin activity, aldosterone and cortisol were determined by the following stimualtions with 3 days of sodium restriction and 2 hours of upright posture, angiotensin II infusion (at a dose which increased 20mmHg of diastolic blood pressure), ACTH administration (rapid i.m. injection of 0.25 mg of alpha 1-24 preparation) and potassium infusion (30 meq of potassium i.v.). Responses of aldosterone in normal-renin hypertensives to all stimulations were 3-5 fold increases from bases line values. Low-renin hypertensives except two of four non-responders showed the responses similar to those in normal-renin patients. The responses of two of the non-responders were similar to those in DOC excess hypertensives who showed reduced responses of aldosterone to some of these stimulations. Thus, it seems that low-renin hypertension is a clinical entity caused by a variety of mechanisms, and the mechanism by which low-renin hypertension is induced is not explained by one factor such as an unknown mineralocorticoid.
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Saito et al. (1976) conducted an observational in Essential hypertension (n=67). Low-renin hypertension vs. Normal-renin hypertension was evaluated on Aldosterone response to physiological stimulations (sodium restriction, upright posture, angiotensin II, ACTH, potassium). Low-renin hypertensive patients showed aldosterone responses to physiological stimulations similar to normal-renin patients (3-5 fold increases), indicating multiple underlying mechanisms.
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