(Hypertension. 2001;37:1315.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Differential Expression of Voltage-Gated K+ Channel Genes in Arteries From Spontaneously Hypertensive and Wistar-Kyoto Rats
From the Department of Physiology, University of Pennsylvania (R.H.C.), Philadelphia; and Department of Pharmacology, Merck Research Laboratories (K.F., R.S.), West Point, Penn.
Correspondence to Robert H. Cox, PhD, Lankenau Institute for Medical Research, 100 Lancaster Ave, Wynnewood, PA 19096.
Abstract—Voltage-gated
K+ currents play an important role in
determining membrane potential, intracellular
Ca2+, and contraction in
arterial smooth muscle. In this study, the expression of
genes encoding voltage-gated K+ channels of
the Kv1.X family was compared in arteries from spontaneously
hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). Expression of
Kv1.X in thoracic aorta, mesenteric arteries, tail artery, and heart
was determined, both qualitatively and quantitatively, by reverse
transcription–polymerase chain reaction. Our results demonstrate
distinct but overlapping patterns of expression in vascular tissues. In
general, Kv1.2 and Kv1.5 were most highly represented, and
the levels of Kv1.2 were significantly larger in all tissues from SHR.
Levels of Kv1.5 in arteries did not differ significantly between
strains but were greater in SHR heart. Moderate levels of Kv1.3 and
Kvß1.1 expression were also found in all tissues and were larger in
SHR. Kv1.1 expression was not different between the 2 strains, and no
significant expression of Kv1.4 (except in heart and aorta), Kv1.6, or
Kvß2.1 was observed in either strain. Kv1.2 and Kv1.5 transcripts
represent 
1 to 2 parts/105 of
total mesenteric arterial RNA with 2- to 5-fold lower
levels in aorta and tail artery. Whole-cell voltage-gated
K+ channel currents, recorded from
mesenteric arterial myocytes, were larger in SHR than WKY
(eg, at 0 mV: 7.3±0.8 versus 10.9±1.2 pA/pF). The voltage dependence
of activation was more negative in SHR (V0.5:
-20±4 mV versus -32±3 mV) but that of availability was not
different. These results indicate that Kv1.X genes are differentially
expressed between WKY and SHR (especially Kv1.2 and Kvß1.1). These
differences in gene expression are associated with a greater
voltage-gated K+ channel current density in
SHR and shifted voltage-dependent activation compared with WKY. These
differences may be a compensatory mechanism related to the membrane
potential depolarization in SHR or some manifestation
thereof.
Key Words: potassium channels • gene expression • hypertension, genetic • arteries • Shaker potassium channels
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