intracellular Ca2+ and force generation determined in resistance arteries of normotensive and hypertensive rats

    loading  Checking for direct PDF access through Ovid



Dysfunctional 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.


A 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.


No 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.


The 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.

Related Topics

    loading  Loading Related Articles