Mesenteric artery contractile properties during dietary calcium manipulation in spontaneously hypertensive and Wistar Kyoto normotensive rats.

The hypothesis that elevated Ca2+ intake lowers blood pressure in the spontaneously hypertensive rat (SHR) by altering intrinsic contractile properties of vascular smooth muscle was tested. The effect of 0.5, 1, and 2% Ca2+ in the diet on systolic blood pressure, serum-ionized Ca2+, and contractile properties of mesenteric arteries isolated from SHR and normotensive Wistar-Kyoto (WKY) rats maintained on diets for 6 and 12 weeks was examined. Blood pressure was significantly elevated in SHR on 0.5% Ca2+ diets after both 6 and 12 weeks, as well as in WKY receiving 1% Ca2+. After six weeks on the diets for the SHR and 6 and 12 weeks for the WKY, serum-ionized Ca2+ was a function of the amount of Ca2+ in the diet. When contractile force generation in response tp KCl or norepinephrine was examined, small diet-related differences were detected, but no consistent linear effect associated with the level of Ca2+ in the diet was observed in either strain. When the sensitivity of the vessels to KCl and norepinephrine was examined, no effects of oral Ca2+ intake were detected. The results indicate that oral Ca2+ loading has modest effects on blood pressure at both 12 and 18 weeks of age in the SHR and WKY and in the younger rat, where Ca2+ intake modulates serum ionized Ca2+ levels. At no age does modification of Ca2+ intake have a consistent effect on mesenteric artery sensitivity or force-generating ability in response to KCl or norepinephrine. These findings do not support the hypothesis that oral Ca2+ loading lowers blood pressure in the rat by altering intrinsic contractile properties of vascular smooth muscle.