Diuretic effect of nitrendipine contributes to its antihypertensive efficacy: a review.

The mechanism of the antihypertensive effect of nitrendipine is believed to be vasodilation, resulting in a reduction of the total peripheral resistance. However, in contrast to other arteriolar vasodilators, nitrendipine exerts natriuretic and diuretic effects that are more pronounced in hypertensive than in normotensive rats. In rat kidneys, nitrendipine caused a complete reversal of the decrease of glomerular filtration rate (GFR) induced by norepinephrine or angiotensin II, probably due to a selective antagonism of preglomerular vasoconstriction. A selective dilation of afferent arterioles was shown in microcirculatory studies on hydronephrotic kidneys. In normotensive rats with intact kidneys, nitrendipine increases natriuresis by inhibition of sodium reabsorption, presumably in the proximal tubuli. In normotensive humans, natriuresis was enhanced also by a primary tubular effect of nitrendipine. In hypertensive patients, an initial increase in GFR was observed; a persistent diuretic effect under chronic treatment was due to a tubular action. In spontaneously hypertensive rats (SHR), chronic treatment with nitrendipine resulted in a regression of cardiac hypertrophy in parallel with a reduction of plasma levels of atrial natriuretic peptides (ANPs), probably due to the persistent natriuretic effect. Treatment with minoxidil resulted in fluid retention, increase in ANP levels, and aggravation of cardiac hypertrophy.