Aggravation of salt-induced hypertension in dahl rats by 2% supplemental dietary calcium

Abstract

There is considerable interest in the antihypertensive potential of supplemental dietary calcium in salt-sensitive hypertension. Previously we reported that very high dietary calcium (4.0% vs. 0.4%) lowers mean arterial pressure in Dahl salt-sensitive (DS) hypertensive rats. However, we have recently observed that more moderate calcium supplementation (2.0% vs. 0.4%) increases mean arterial pressure in DS rats. To further evaluate the pressor action of 2.0% versus 0.4% calcium, we tested for effects of 2.0% calcium in female DS rats fed low (0.2%), moderate (1.0%), and high (2.7%) sodium and in Dahl salt-resistant (DR) rats fed high sodium from 6 to 12 weeks old («=10-13 rats per group). At 12 weeks, 2.0% calcium increased mean arterial pressure and the cardiac ventricular weight/body weight ratio in DS rats fed high sodium (p<0.05) but not in DS rats fed low or moderate sodium or in DR rats fed high sodium. Ganglionic blockade decreased mean arterial pressure in all groups but failed to abolish or attenuate the difference in mean arterial pressure between high sodium-fed DS rats on 2.0% and 0.4% calcium diets. In the same DS rats fed a high sodium diet, 2.0% calcium increased systemic pressor responsiveness to graded norepinephrine administration after ganglionic blockade. Thus, 2.0% supplemental calcium intake enhances salt-induced hypertension in DS rats. This prohypertensive action of 2.0% calcium is dependent on a critically high level of between 1.0% and 2.7% sodium in the diet. The mechanism of this prohypertensive action of 2.0% calcium does not appear to be either increased sympathetic neural activity or increased responsiveness to norepinephrine since it remains intact after ganglionic blockade. The present study provides evidence that dietary calcium supplementation has the potential for increasing arterial pressure even in a model of hypertension induced by high dietary salt. © 1989 American Heart Association, Inc.