CALCIUM CURRENT IN SMOOTH-MUSCLE CELLS FROM NORMOTENSIVE AND GENETICALLY HYPERTENSIVE RATS

Genetic hypertension results from numerous phenotypic expressions. We hypothesized that increased calcium current in vascular smooth muscle of genetically hypertensive animals is partly responsible for observed increases in agonist sensitivity, contractility, and calcium influx. Using adult, spontaneously hypertensive stroke-prone rats (SHRSP) and normotensive Wistar-Kyoto (WKY) controls from an inbred colony, we cha racterized calcium current in smooth muscle cells isolated from cerebr al arteries. Calcium current in WKY cells reached a maximum of -27.7+/ -2.7 pA (n=32) at +20 mV. Peak inward current at +20 mV in SHRSP cells had a mean amplitude of -44.4+/-3.0 pA (n=72, P<.05). SHRSP cells exh ibited a higher calcium current density. Maximal inward current normal ized to cell capacitance yielded mean values of 2.07+/-0.11 pA/pF for WKY (n=32) and 2.80+/-0.12 pA/pF (n=79) for SHRSP (P<.05) cells. Trans ient-type Ca2+ channel current had the same magnitude and current-volt age relation in both cell types, giving an L-type/T-type ratio of 3.85 for WKY and 6.25 for SHRSP cells. The voltage-dependent inactivation curve for SHRSP calcium current was shifted to the right only over the range of -50 to -30 mV, but the half-maximal inactivation voltages an d Boltzmann coefficients were not significantly different between cell types. Increased calcium inward current in this model of genetic hype rtension could account in part for altered calcium homeostasis and inc reased vascular reactivity, contributing to hypertension and vasospasm .