Abstract
Arterial potassium permeability is increased in hypertension. In this study we conducted voltage-clamp experiments to determine whether the whole-cell K+ current is increased in a Ca(2+)-dependent manner in aortic smooth muscle cells from stroke-prone spontaneously hypertensive rats (SHRSP). Aortic cells from Wistar-Kyoto (WKY) rats and SHRSP demonstrated an outward rectifying current elicited by depolarization. The current was carried primarily by K+, because intracellular Cs+ replacement eliminated more than 97% of the current. The current density was higher (P < .05) in SHRSP cells at positive potentials. In the presence of LaCl3 (200 mumol/L) or tetraethylammonium (10 mmol/L), the residual current was similar in WKY and SHRSP cells. Also, the current density did not differ between WKY and SHRSP cells in which the intracellular Ca2+ concentration was clamped at zero. Fura 2 ratio measurement showed similar resting myoplasmic Ca2+ concentration (Ca2+m) in WKY and SHRSP cells (100 +/- 10 versus 117 +/- 9 nmol/L, P = .2). Under low extracellular Na+ conditions, which had a minimal effect on Ca2+m, Ba2+ replacement of Ca2+ caused a continuous and approximately linear increase in the fura 2 ratio, which was twofold faster in SHRSP cells. Because Ca2+ pumps do not transport Ba2+ and Na(+)-Ca2+ exchange was inhibited by low extracellular Na+, this increase reflected unidirectional Ba2+ influx.(ABSTRACT TRUNCATED AT 250 WORDS)