Key result
Azelnidipine treatment for 4 weeks significantly reduced blood pressure without significantly altering plasma renin activity (p=0.42) or plasma aldosterone concentration (p=0.12) in drug-naïve hypertensive patients.
Why the study?
Does azelnidipine affect plasma renin activity and plasma aldosterone concentration in hypertensive patients?
Does azelnidipine affect plasma renin activity and plasma aldosterone concentration in hypertensive patients?
Absolute Event Rate: 1.45% vs 1.19%
p-value: p=0.42
Azelnidipine effectively lowers blood pressure without stimulating plasma renin activity or plasma aldosterone concentration, making it a suitable antihypertensive agent to use during screening for primary aldosteronism.
Azelnidipine may lower BP without PRA/PAC changes; leaves open suitability for primary aldosteronism screening pending randomized trials.
OBJECTIVE: In hypertensive patients, primary aldosteronism (PA) is the most prevalent type of secondary hypertension, and screening for PA has become very important. Calcium channel blockers (CCB) are widely used to treat hypertension, but most CCBs stimulate plasma renin activity (PRA) and increase plasma aldosterone concentration (PAC), both of which are used in the screening for PA. The aim of this study was to determine whether the newly introduced CCB, azelnidipine, affects PRA and PAC. METHODS: 40 hypertensive patients were treated with 16 mg of azelnidipine for 4 weeks. RESULTS: Azelnidipine treatment in drug-naïve (DN) cases significantly decreased systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR). PRA and PAC in the DN group on azelnidipine treatment were indistinguishable from those in the DN group before treatment. Compared with other CCB treatments such as amlodipine, manidipine and slow-release nifedipine, azelnidipine showed comparable or significant reductions in SBP, DBP and HR. In patients who were switched from other CCBs to azelnidipine, PRA and PAC were decreased, except for PAC on amlodipine treatment. Since the PRA reduction rate exceeded that of PAC, the aldosterone/renin ratio (ARR) was significantly increased in those on azelnidipine treatment who had been switched from manidipine or nifedipine treatment, suggesting the restoration of possibly underestimated ARR values. CONCLUSION: These data indicate that azelnidipine does not affect PRA or PAC, suggesting that azelnidipine could be a useful antihypertensive CCB while undergoing PA screening.
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Kondo et al. (2010) studied Hypertension (n=40). Azelnidipine vs. Baseline (pre-treatment or prior calcium channel blocker) was evaluated on Plasma renin activity (PRA) in drug-naïve patients (ng/mL/h) (p=0.42). Azelnidipine treatment for 4 weeks significantly reduced blood pressure without significantly altering plasma renin activity (p=0.42) or plasma aldosterone concentration (p=0.12) in drug-naïve hypertensive patients.
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