INCREASED BARIUM INFLUX AND POTASSIUM CURRENT IN STROKE-PRONE SPONTANEOUSLY HYPERTENSIVE RATS

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 Ca2+-dependent manner in aorti c smooth muscle cells from stroke-prone spontaneously hypertensive rat s (SHRSP). Aortic cells from Wistar-Kyoto (WKY) rats and SHRSP demonst rated an outward rectifying current elicited by depolarization. The cu rrent was carried primarily by K6+, because intracellular Cs+ replacem ent eliminated more than 97% of the current. The current density was h igher (P<.05) in SHRSP cells at positive potentials. In the presence o f LaCl3 (200 mu mol/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 show ed similar resting myoplasmic Ca2+ concentration (Ca-m(2+)) in WKY and SHRSP cells (100+/-10 versus 117+/-9 nmol/L, P = .2). Under low extra cellular Na+ conditions, which had a minimal effect on Ca-m(2+), Ba2replacement of Ca2+ caused a continuous and approximately linear incre ase in the fura 2 ratio, which was twofold faster in SHRSP cells. Beca use Ca2+ pumps do not transport Ba2+ and Na+-Ca2+ exchange was inhibit ed by low extracellular Na+, this increase reflected unidirectional Ba 2+ influx. These results suggest that (1) Ca2+-dependent K+ channel ac tivity is increased in aortic smooth muscle cells from SHRSP, probably as a result of an increased Ca2+ influx that does not cause an increa se in Ca-m(2+), and (2) increased Ca2+ cycling, which may underlie the increased K+ current, may occur across the sarcolemma in SHRSP cells.