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on membrane currents
in rabbit middle cerebral arterial smooth muscle cells
Department of Physiology and Biophysics, College of Medicine, Inje University, Busanjin-gu, Busan, 614-735, Korea
Although PGF2
affects contractility of vascular smooth muscles, no studies to date
have addressed the electrophysiological mechanism of this effect. The
purpose of our investigation was to examine the direct effects of
PGF2
on membrane potentials, Ca2+-activated
K+ (KCa) channels, delayed rectifier
K+ (KV) channels, and L-type Ca2+
channels with the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells (SMCs). PGF2
significantly hyperpolarized membrane potentials and increased the
amplitudes of total K+ currents. PGF2
increased open-state probability but had little effect on the open and
closed kinetics of KCa channels. PGF2
increased the amplitudes of KV currents with a leftward shift of the activation and inactivation curves and a decrease in the
activation time constant. PGF2
decreased the amplitudes of L-type Ca2+ currents without any significant change in
threshold or apparent reversal potentials. This study provides the
first finding that the direct effects of PGF2
on middle
cerebral arterial SMCs, at least in part, could attenuate vasoconstriction.
membrane currents; Ca2+-activated K+ channels; delayed rectifier K+ channels; Ca2+ channels
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