High oral potassium (K) decreases stroke incidence in aging high salt-fed stroke-prone spontaneously hypertensive rats (SHRSP). We have seen high oral Ca increase stroke incidence in aging high salt-fed SHRSP without increasing blood pressure (BP) but with signs of K wasting. Therefore, we sought to determine whether high oral Ca suppresses the previously reported oral K-related enhancement of arterial endothelium-dependent relaxation as seen in younger high salt-fed SHRSP before the appearance of strokes. Four groups of female SHRSP were fed high-salt diets containing either low (0.4%) or high (1.6%) K with low (0.4%) and high (1.6%) Ca from age 1 to 4 mos. High oral K decreased BP independent of Ca intake (P < 0.05). High oral Ca did not affect BP. In contrast to aging SHRSP, high oral Ca neither increased urinary excretion nor decreased plasma concentration of K in these young adult SHRSP. However, high (vs. low) oral K only significantly reduced the half-maximal effective dose for acetylcholine-induced relaxation of aortic rings from rats fed low (18 +/- 3 vs. 38 +/- 6 nM, P < 0.05) not high Ca (25 +/- 5 vs. 31 +/- 3 nM). Neither oral K nor Ca affected nitroprusside-induced relaxation. Thus high oral Ca by itself does not impair endothelium-dependent relaxation in young adult high salt-fed SHRSP, but yet it suppresses the enhancing effect of high oral K on such relaxation and does so without altering BP, K balance, or endothelium-independent relaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Black hypertensive diabetics have been shown to exhibit elevated intracellular calcium which may stimulate Na/H antiport. Since Na/Li countertransport appears to be a functional mode of Na/H antiport, we measured erythrocyte Na/Li countertransport in nondiabetic normotensive and hypertensive blacks and whites and hypertensive non-insulin-dependent diabetic blacks. Na/Li countertransport was significantly lower in the blacks than in the whites (0.170 +/- 0.017 v 0.230 +/- 0.017 mmol/L/h, P less than .02), but there was no significant difference between the black hypertensives and normotensives. In contrast, black hypertensive diabetics exhibited a significant increase in Na/Li countertransport compared to normotensive and hypertensive nondiabetic blacks (0.252 +/- 0.032 v 0.170 +/- 0.017, P less than .02. Thus, these data indicate that the activity of this antiporter is elevated in black diabetics, possibly further contributing to the development of hypertension in this population.