High calcium diet reduces blood pressure in dahl salt-sensitive rats by neural mechanisms

Abstract

We tested the hypothesis that high dietary calcium attenuates hypertension in Dahl salt-sensitive rats by neural as opposed to vascular mechanisms. Four-week-old Dahl salt-sensitive rats were fed a high salt diet (3.3% sodium) with either high (4.0%; n = 21) or normal (0.4%; n = 21) calcium content until they were 10 to 11 weeks old. Total plasma calcium concentration was increased and plasma phosphorus concentration was decreased by the high calcium diet. At 10 weeks, food intake and intestinal absorption of sodium were not altered by the high calcium diet. There were three major observations. First, mean arterial pressure was lower in awake rats fed a high versus normal calcium diet (137 ± 7, n = 11, vs 165 ± 6 mm Hg, n = 10, respectively; p < 0.05). This pressure difference was dependent on intact autonomic transmission, since ganglionic blockade eliminated the significant difference between pressures in rats fed high (78 ± 5 mm Hg) and normal (85 ± 6 mm Hg) calcium diets. Second, high calcium intake augmented baroreceptor reflex inhibition of renal sympathetic nerve activity and heart rate during ramp increase in arterial pressure produced by infusion of phenylephrine. Reflex suppression of renal sympathetic nerve activity was twofold greater in rats fed the high (vs normal) calcium diet (-2.79 ± 0.25 vs -1.34 ± 0.14 %Δ/Δ mm Hg, respectively; n = 9 rats per group; p < 0.05). Third, high calcium intake did not attenuate vascular responsiveness, since pressor responses to norepinephrine and angiotensin II did not differ between rats fed high and normal calcium diets after ganglionic blockade. In conclusion, we found that high calcium feeding attenuated salt-induced hypertension in Dahl salt-sensitive rats by reducing the neural contribution to hypertension rather than by reducing vascular responsiveness to vasoconstrictor stimuli. © 1987 American Heart Association, Inc.