• The Korean Journal of Physiology and Pharmacology
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• v.3 no.6
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• pp.547-554
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• 1999

The aim of the present study is to investigate the contribution of $Ca^{2+} ?activated\;K^+\;(K_{Ca})$ channels and delayed rectifier $K^+\;(K_V)$ channels to the resting membrane potential (RMP) in rabbit middle cerebral arterial smooth muscle cells. The RMP and membrane currents were recorded using the whole-cell patch configuration and single $K_{Ca}$ channel was recorded using the outside-out patch configuration. Using the pipette solution containing 0.05 mM EGTA, the RMP was $-25.76{\pm}5.08$ mV (n=12) and showed spontaneous transient hyperpolarizations (STHPs). The membrane currents showed time- and voltage-dependent outward currents with spontaneous transient outward currents (STOCs). When we recorded the membrane potential using the pipette solution containing 10 mM EGTA, the RMP was depolarized and did not show STHPs. The membrane currents showed no STOCs but only showed slowly inactivating outward currents. External TEA (1 mM) reversibly inhibited the STHPs, depolarized the RMP, reduced the membrane currents, abolished STOCs, and decreased the open probability of single $K_{Ca}$ channel. When $K_V$ currents were isolated, the application of 4-AP (5 mM) depolarized the RMP. The important aspect of our results is that $K_{Ca}$ channel is responsible for the generation of the STHPs in the membrane potential and plays an important role in the regulation of the RMP and $K_V$ channel is also responsible for the regulation of the RMP in rabbit middle cerebral arterial smooth muscle cells.

• The Korean Journal of Physiology and Pharmacology
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• v.4 no.4
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• pp.301-309
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• 2000

The purpose of our investigation was to examine the effects of prostaglandin $F_{2{\alpha}}\;(PGF_{2{\alpha}})$ on membrane potentials, $Ca^{2+}-activated\;K^+\;(K_{Ca})$ channels, and delayed rectifier $K^+(K_V)$ channels using the patch-clamp technique in single rabbit middle cerebral arterial smooth muscle cells. $PGF_{2{\alpha}}$ significantly hyperpolarized membrane potentials and increased outward whole-cell K currents. $PGF_{2{\alpha}}$ increased open-state probability of $K_{Ca}$ channels without the change of the open and closed kinetics. $PGF_{2{\alpha}}$ increased the amplitudes of $K_V$ currents with a leftward shift of activation and inactivation curves and a decrease of activation time constant. Our results suggest that the activation of $K_{Ca}$ and $K_V$ channels, at least in part, may lead to attenuate or counteract vasoconstriction by $PGF_{2{\alpha}}$ in middle cerebral artery.