Cardiovascular effects of felodipine are not antagonized by dietary salt

Abstract

Increased dietary intake of regular salt (sodium chloride) interferes markedly with the therapeutic effects of angiotensin converting enzyme inhibitors. To study further the interactions between dietary salt intake and antihypertensive drug treatment, we examined the effects of felodipine, a dihydropridine derivative Ca 2+ channel antagonist with natriuretic properties, on blood pressure and the development of left ventricular hypertrophy in the stroke-prone spontaneously hypertensive rats during different levels of sodium chloride in the diet. We also compared the influence of regular salt on the cardiovascular effects of felodipine with that of a novel K +-, Mg 2+- and l-lysine-enriched and Na +-reduced salt alternative, which in previous studies markedly improved the therapeutic effects of enalapril and ramipril. During the 28-day experiment regular salt produced a marked rise in blood pressure and induced left ventricular hypertrophy, while the salt alternative neither induced any rise of blood pressure nor caused cardiac hypertrophy. Felodipine had an enhanced antihypertensive effect during the increased intake of sodium chloride, and lowered the blood pressure to the same normotensive level as it did during the control and the salt alternative diets. Felodipine also completely blocked the development of the sodium chloride-induced cardiac hypertrophy. The heart rate of the felodipine-treated animals was significantly increased during the first two study weeks but thereafter it did not differ from that of the controls. Hence, unlike regular salt, the novel Na +-reduced, K +-, Mg 2+-, and l-- lysine- enriched salt alternative did not raise blood pressure and produced little if any left ventricular hypertrophy. Felodipine lowered blood pressure even in the presence of a high intake of salt.