Contrasting hemodynamic effects of high oral calcium in genetic models of salt-sensitive hypertension.

Interest in effects of oral calcium (Ca) on blood pressure is now generally focused on salt-induced hypertension. In this study hemodynamic effects of long-term high oral Ca were examined in two different genetic models of salt-sensitive hypertension, stroke-prone spontaneously hypertensive rats (spSHR) and Dahl salt-sensitive (DS) hypertensive rats. High vs low oral Ca (2.0 vs 0.4% Ca, 8-13 rats/diet) significantly (p less than 0.05) attenuated salt-induced hypertension (7% NaCl intake) in female spSHR (mean arterial pressure = 137 vs 175 mmHg) but aggravated such hypertension in female DS rats (141 vs 124 mmHg). Pressor responsiveness to norepinephrine (NE) and angiotensin (A) II were examined in the same rats. High oral Ca decreased pressor responses to graded intravenous injections of NE and AII in spSHR and increased such responses in DS rats. In spSHR, the decreased pressor responsiveness preceded the antihypertensive effect of high oral Ca. In summary, 2.0 vs 0.4% oral Ca produces contrasting effects on blood pressure in two genetic models of salt-sensitive hypertension (stroke-prone SHR and Dahl salt-sensitive rats). These contrasting effects on blood pressure may be related to differential effects of oral Ca on vascular responsiveness to endogenous vasoconstrictors in these two genetic models of salt-sensitive hypertension.