EFFECTS OF ORAL CALCIUM AND POTASSIUM ON ENDOTHELIUM-DEPENDENT RELAXATION IN HYPERTENSIVE RATS

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 w ithout increasing blood pressure (BP) but with signs of K wasting. The refore, we sought to determine whether high oral Ca suppresses the pre viously reported oral K-related enhancement of arterial endothelium-de pendent relaxation as seen in younger high salt-fed SHRSP before the a ppearance of strokes. Four groups of female SHRSP were fed high-salt d iets 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 independ ent of Ca intake (P < 0.05). High oral Ca did not affect BP. In contra st to aging SHRSP, high oral Ca neither increased urinary excretion no r decreased plasma concentration of K in these young adult SHRSP. Howe ver, high (vs. low) oral K only significantly reduced the half-maximal effective dose for acetylcholine-induced relaxation of aortic rings f rom 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-i nduced relaxation. Thus high oral Ca by itself does not impair endothe lium-dependent relaxation in young adult high salt-fed SHRSP, but yet it suppresses the enhancing effect of high oral K on such relaxation a nd does so without altering BP, K balance, or endothelium-independent relaxation. Accordingly, we speculate that high oral Ca may impair the ability of K to protect aging high salt-fed SHRSP against forms of st roke in which endothelial cell dysfunction may play a role.