1994 Volume 17 Issue 1 Pages 59-69
The present high levels of sodium chloride (regular salt, RS) intake interfere with the therapeutic effects of angiotensin converting enzyme inhibitors. In previous studies a novel potassium-, magnesium- and 1- lysine-enriched and sodium-reduced salt alternative (SA) has been virtually devoid of the hypertensive, left ventricular hypertrophy producing, and life-span shortening effects, characteristic of RS. We therefore compared the influence of SA on the cardiovascular effects of enalapril with that of RS in male stroke-prone spontaneously hypertensive rats (SHRSP). During the 28-day experiment, RS alone produced a marked rise in blood pressure, induced remarkable left ventricular hypertrophy, and caused the death of five out of 18 SHRSP. Oral enalapril treatment did not significantly affect either of the detrimental cardiovascular effects of RS but there were no deaths in the enalapril-treated group. The SA supplemented diet neither caused mortality nor induced any significant rise in blood pressure as compared to control SHRSP, and caused significantly less cardiac hypertrophy than RS. During SA, enalapril had a marked antihypertensive effect and it also completely blocked the salt-induced left ventricular hypertrophy. During SA+enalapril or SA alone, there was no tendency to hyperkalemia in any of the SHRSP. There was not any difference in the plasma renin activity (PRA) between control, RS and SA groups. Enalapril increased PRA to the same extent, approximately three-fold, in the RS and in the SA supplemented SHRSP. Hence, PRA does not explain the marked improvement of the effects of enalapril by SA in comparison to RS. Our findings suggest that replacement of regular salt by the novel salt alternative may remarkably improve the cardiovascular effects of enalapril treatment. (Hypertens Res 1994; 17: 59-69)
