Hypertension, Vol 19, 301-307, Copyright © 1992 by American Heart Association
NJ Rusch, RG De Lucena, TA Wooldridge, SK England and AW Cowley Jr
This study was designed to investigate the role and regulation of arterial
membrane K+ channels in hypertension. Aortic segments from normotensive
Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were
suspended for isometric tension recording. In other experiments, proximal
aortic segments (PS) (exposed to high pressure) and distal aortic segments
(DS) (exposed to lower pressure) were removed from surgically coarcted
Sprague-Dawley rats and similarly prepared. Aortas from SHR and PS
dose-dependently contracted to the K+ channel blocker tetraethylammonium
(TEA) (0.1-10 mM), and this contraction was abolished by preincubation with
0.1 microM nifedipine. In contrast, the same concentrations of TEA did not
contract either WKY or DS aortas. Since block of K+ channels by TEA had a
different effect on aortic segments exposed to high versus low blood
pressure, we compared whole-cell K+ currents in isolated vascular cells
from the same aortas. The reversal potentials of depolarization-induced
outward currents in WKY, SHR, DS, and PS aortic cells showed a Nernst
relation to external K+ concentration indicative of selective K+
permeability. TEA (1 and 10 mM) was equipotent in blocking these K+
currents in patch- clamped cells from all aortic preparations, suggesting
that the lack of TEA-induced contractions in WKY and DS aortas was not due
to an absence of TEA-sensitive K+ channels in these arterial membranes.
However, when the Ca2+ ionophore A23187 (10 microM) was used to increase
the level of cytosolic Ca2+ in patch-clamped cells, the K+ current density
in SHR and PS aortic cells was twofold or more higher than in WKY and DS
cells.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
A Ca(2+)-dependent K+ current is enhanced in arterial membranes of hypertensive rats
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
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