Key result
Antihypertensive response to propranolol or chlorthalidone is linked to significantly lower aldosterone levels.
Why the study?
The role of the renin-aldosterone axis in mediating responses to antihypertensive treatment in essential hypertension was examined to clarify its influence on treatment outcomes.
Observational (n=100)
Answers are grounded in this paper and cite their sources.
Lower aldosterone may identify responders to these agents; leaves open whether aldosterone modulation improves hypertension control.
The role of the renin-aldosterone axis in mediating responses to antihypertensive treatment was examined in patients with essential hypertension treated with propranolol (n=50) or chlorthalidone (n=50). Control plasma renin activity tended to be predictive of the response to treatment: it correlated with the diastolic blood pressure changes produced by both the renin-lowering agent, propranolol (r=-.43, P less than 0.001), and the diuretic, chlorthalidone (r= .48, P less than 0.001). However, when patients were divided into responders (fall in diastolic blood pressure of greater than 10%) and non-responders, the treatment-induced changes in aldosterone excretion rate appeared to be more important than the changes in renin in determining outcome. During propranolol there was no difference between the renin changes in the responders (n=21) and the non-responders (n=29), but aldosterone fell significantly more (P less than 0.025) in the responders than in the non-responders. Similarly, renin changes during chlorthalidone were not markedly different between the two groups, but the increase in aldosterone excretion in the non-responders was significantly greater (P less than 0.001) than in the responders (n=25). Thus, regardless of the treatment used, responders were characterized by having lower levels of aldosterone during therapy than non-responders. This possible role for aldosterone in influencing blood pressure changes was not related to clinically measurable effects on fluid and electrolyte balance; it has been conjectured that this pressor effect of aldosterone could reflect a direct action in the peripheral circulation.
No takes yet. Share an insight, caveat, or question.
Weber et al. (1982) conducted an observational in Primary hypertension (essential hypertension) (n=100). Antihypertensive treatment (propranolol or chlorthalidone) vs. Responders vs non-responders was evaluated on Treatment-induced changes in aldosterone excretion rate and plasma renin activity between blood pressure responders and non-responders (p=<0.001). Patients with essential hypertension who responded to propranolol or chlorthalidone therapy had significantly lower aldosterone levels during treatment compared to non-responders.
Synapse has enriched 10 related papers. Consider them for comparative context: