Abstract

The effects of oral calcium loading on the development of hypertension were studied in spontaneously hypertensive rats (SHR). Forty-eight male SHR were divided into four groups according to treatment: control, calcium, deoxycorticosterone (DOC) and DOC + calcium. Both calcium groups received ad libitum 1.5% CaCl2 as drinking fluid. The DOC animals were injected with a mineralocorticoid, deoxycorticosterone trimethyl-acetate, 25 mg/kg, s.c., once a week. Systolic blood pressure (BP) was measured once a week by the tail cuff method. During the nine-week study, the development of hypertension was enhanced in the DOC group, while in the calcium group a blood pressure-lowering effect was observed when compared to the controls. Calcium also abolished the hypertensive effect of DOC. The maximal velocity of calcium transport was higher in "inside-out"-vesicles of red blood cells as compared to controls in both calcium-supplemented groups. DOC treatment resulted in elevated sodium and potassium contents in tail artery tissue, while the effect of the combination of DOC + calcium was equal to controls. On the other hand, the tissue Na:K ratio was decreased in both tail artery wall and heart in the calcium group. Calcium treatment diminished the excretion of phosphate in both groups, while the plasma phosphate concentration was lowered in the calcium group. In mesenteric arterial rings, DOC impaired nitroprusside-induced relaxation, while the relaxation was enhanced compared to control in both the calcium and DOC + calcium groups.(ABSTRACT TRUNCATED AT 250 WORDS)

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