(Hypertension. 1997;30:1403-1409.)
© 1997 American Heart Association, Inc.
Articles |
Increased Expression of Ca2+-Sensitive K+ Channels in Aorta of Hypertensive Rats
From the Department of Physiology (Y.L., K.P., N.J.R.), Medical College of Wisconsin (Milwaukee), and Institute for Biochemical Pharmacology (H.-G.K.), Innsbruck, Austria.
Correspondence to Nancy J. Rusch, PhD, Associate Professor, Department of Physiology, Medical College of Wisconsin, 8701 Watertown Plank Rd, Milwaukee, WI 53226. E-mail nrusch{at}post.its.mcw.edu
Abstract Potassium efflux through Ca2+-sensitive
K+ channels (KCa channels) is increased in
arterial smooth muscle cells from hypertensive rats, but
the molecular mechanism is unknown. The goal of this study was to
compare the levels of KCa channel current between aortic
smooth muscle cells from adult Wistar-Kyoto rats (WKY) and
spontaneously hypertensive rats (SHR) and then use Western blot methods
and ribonuclease protection assays to examine the expression and mRNA
levels for the KCa channel in these same vascular tissues.
Whole-cell patch-clamp methods indicated a larger component of
KCa channel current, sensitive to block by iberiotoxin (100
nmol/L), in single aortic smooth muscle cells from SHR compared with
WKY. Subsequent Western blot analysis using a site-specific
antibody (anti–
913–926) directed against the S9/S10
linker of the -subunit of the KCa channel revealed a
125-kD immunoreactive band in lanes loaded with either WKY or SHR
aortic muscle membranes. The immunoreactive density of this band, which
corresponded to the known molecular size of the -subunit, was
2.2-fold greater in lanes loaded with aortic smooth muscle membranes
from the hypertensive animals. However, despite this evidence for an
increased expression and functional enhancement of KCa
channels in aortic smooth muscle membranes of SHR, ribonuclease
protection assays with a 32P-labeled riboprobe targeted
against the S9/S10 linker of the KCa channel -subunit
revealed no difference in mRNA levels for the -subunit between WKY
and SHR aortic tissue. These findings provide initial evidence that (1)
an increased expression of KCa channels may be a mechanism
for the enhanced KCa current in aortic smooth muscle
membranes of SHR, and (2) the upregulation of KCa channels
in arterial muscle membranes during hypertension, which is
regarded as a homeostatic mechanism for buffering vascular
excitability, may rely on post-transcriptional events.
Key Words: vascular smooth muscle • K+ channel • ion channel expression • iberiotoxin
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