The effect of diltiazem hydrochloride upon sodium diuresis and renal function in chronic congestive heart failure.

d-3-Acetoxy-cis-2,3-dihydro-5-]2-(dimethylamino)ethyl]-2-(p-methoxyphenyl)-1,5-benzothiazepin-4(5H)-one hydrochloride (diltiazem HCl) was orally administered to 9 patients with chronic congestive heart failure (Class IIb to III, NYHA) to examine whether the drug induces sodium retention and aggravates congestive heart failure. Renal hemodynamics and urinary electrolytes excretion were measured for 3 h after the medication in 6 out of 9 patients. Four of the rest of patients had received chronic administration of the drug for about 2 weeks. There was a significant increase in urinary sodium excretion without noticeable change in renal hemodynamics after diltiazem administration, demonstrating the presence of its direct inhibitory action on renal tubules. The increase in urinary sodium excretion was more marked in patients with heart failure than in those without. This difference in the response to diltiazem may be due to the functional constriction of renal cortical vessels in heart failure. This constriction may be related to renin-angiotensin system which diltiazem was reported to antagonize. The chronic administration of the drug did not induce sodium retention and edema. There was no deterioration of symptoms due to congestive heart failure such as dyspnea and body weight increase. It may be concluded that diltiazem does not aggravate congestive heart failure through its diuretic action and probably its systemic vasodilating action.