The renoprotective effects of benidipine, a calcium channel blocker (CCB) developed in Japan, are reviewed
herein. Benidipine has a sustained antihypertensive effect independent of its blood concentration since it binds to
dihydropyridine (DHP) receptors via a “membrane approach” (approach to the cell membrane followed by long retention
at the DHP binding site). Benidipine dilates glomerular afferent and efferent arterioles equally through inhibition of Ttype
Ca channels. Thus, it may cause a decrease of intraglomerular pressure and is superior to CCBs (capable of inhibiting
only L-type Ca channels) in terms of suppression of proteinuria. Additionally, benidipine suppresses worsening of renal
function more powerfully than CCBs (suppressing only L-type Ca channels), allowing better prognosis as to renal
function. The inhibitory effect of benidipine on T-type calcium channels results in the suppression of aldosterone
formation in the adrenal glands and of oxidative stress induced by aldosterone. Thus, the aldosterone-inhibitory and
antioxidant activities of benidipine mediated by inhibition of T-type calcium channels would result in renoprotection and
suppression of disease progression in hypertensive patients with chronic kidney disease (CKD). If such patients have
proteinuria, renin-angiotensin system (RAS) inhibitors are used as first-line drugs, but benidipine, as an L-/T-type CCB, is
recommended when they require some concomitant drugs. Moreover, the superiority of RAS inhibitors has not been
demonstrated in hypertensive patients with CKD and without proteinuria. Thus, in such patients, benidipine should be
considered as a first-line antihypertensive drug.
Benidipine, chronic kidney disease, hypertension, L-/T-type CCBs, renoprotective effects.
Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, Tokyo 113-8421, Japan.