ObjectiveDysfunctional cellular Ca2+handling has been proposed to underlie the heightened vascular reactivity observed in the spontaneously hypertensive rat (SHR) model of genetic hypertension. We tested the hypothesis that basal or agonist-induced mobilization of intracellular Ca2+is elevated in mesenteric resistance arteries of SHR compared with the normotensive Wistar-Kyoto (WKY) rat.DesignA method using fura-2 for the simultaneous measurement of intracellular Ca2+and isometric force generation in isolated mesenteric resistance arteries was employed to measure agonist-induced changes in Ca2+and force during activation with 100 μol/I K+or 10 μmol/I norepinephrine. Arteries with normalized diameter 220–240μm from male rats aged 14–15 weeks were examined.ResultsNo differences were detected between the rat strains in basal Ca2+ concentration or the steady-state concentration of Ca2+achieved in response to either 100 mmol/I K+or 10 μmol/I norepinephrine. The relationship between Ca2+ and force during the contractile responses to K+and norepinephrine was analyzed. No differences between the strains in the level of active stress, normalized to unit intracellular Ca2+, were detected in the steady-state responses to K+or norepinephrine.ConclusionsThe present results do not support the hypothesis that alterations in either the basal concentration of intracellular Ca2+or the amount of intracellular Ca2+mobilized in response to high levels of norepinephrine or K+are present in resistance arteries of SHR compared with those of WKY rats. Moreover, these findings suggest that elevations in Ca2+do not contribute to heightened peripheral resistance in SHR.