Hypertension, Vol 24, 739-746, Copyright © 1994 by American Heart Association
DW Wilde, PB Furspan and JF Szocik
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
characterized calcium current in smooth muscle cells isolated from cerebral
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
exhibited a higher calcium current density. Maximal inward current
normalized 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. Transient-type Ca2+ channel current had the same magnitude and
current-voltage 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
and Boltzmann coefficients were not significantly different between cell
types. Increased calcium inward current in this model of genetic
hypertension could account in part for altered calcium homeostasis and
increased vascular reactivity, contributing to hypertension and vasospasm.
ARTICLES
Calcium current in smooth muscle cells from normotensive and genetically hypertensive rats
Department of Anesthesiology, University of Michigan Medical School, Ann Arbor.
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