High calcium diet effectively opposes the development of deoxycorticosterone-salt hypertension in rats.

The effects of increased dietary calcium intake on blood pressure and arterial function were investigated in one-kidney deoxycorticosterone-salt hypertensive Wistar rats. The calcium content of the control diet was 1.1%, and that of the high calcium diet, 2.5%. During the 10-week study calcium supplementation markedly attenuated the steroid-salt-induced rise in blood pressure and the associated cardiac hypertrophy. Responses of mesenteric arterial rings in vitro were examined at the end of the study. In deoxycorticosterone-salt-treated rats, the contractile sensitivity of endothelium-denuded preparations to norepinephrine, 5-hydroxytryptamine, and KCl, and the inhibitory effect of nifedipine on KCl-evoked responses were enhanced. It is interesting that the high calcium diet alleviated the steroid-salt-induced increase in sensitivity to KCl but did not significantly affect it to the receptor-mediated agonists norepinephrine and 5-hydroxytryptamine. Thus, sensitivity to membrane depolarization was reduced by calcium supplementation. Smooth muscle responses were also studied by challenging the preparations with KCl in a calcium-free solution, after which calcium was added to the organ bath in increasing concentrations. In steroid-salt-treated rats, these calcium contractions were attenuated, but concomitant calcium supplementation normalized the responses, suggesting improved cell membrane handling of calcium. In addition, the mineralocorticoid-salt treatment impaired relaxation responses of endothelium-intact arterial rings to acetylcholine, sodium nitroprusside, and isoproterenol.(ABSTRACT TRUNCATED AT 250 WORDS)