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KMID : 0811720000040000014
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Korean Journal of Physiology & Pharmacology
2000 Volume.4 No. 0 p.14 ~ p.0
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Characterization of Ca2+-activated Currents and their Regulation by [Mg2+]i in Rabbit Coronary Artery Smooth Muscle Cells
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Bae Young-Min
Kim Ki-Suk
Ko Eun-A
Lee Suk-Ho
Ho Won-Kyung
Earm Yung-E
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Abstract
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Cytosolic Ca2+ not only regulates vascular tone, but also regulates membrane potential by its action on Ca2+-activated ion channels. From this, we can infer the presence of feedback mechanism for regulation of [Ca2+]i in vascular smooth muscle. We investigated the ionic nature of Ca2+-activated currents and modulation of these currents by [Mg2+]i in rabbit coronary arterial smooth muscle cells (CASMCs). Membrane currents were recorded using the whole-cell voltage clamp technique. To induce [Ca2+]i transient, caffeine was briefly applied. At Vhold = -50 mV, caffeine elicited outward or inward currents, and the reversal potential (Vrev) of these currents was in the range from -70 mV to -12 mV. In K+-free condition, however, caffeine elicited only inward current. Vrev of this current was near 0 mV. Replacement of bath Na+ with membrane-impermeable N-methyl D glucamine little affected on the Vrev and amplitude of the inward current. Niflumic acid, a Ca2+-activated Cl- (ClCa) channel blocker suppressed the current. When [Mg2+]i was low (0.1 mM), amplitude of Ca2+-activated K+ current (IKCa) was small (14±6 pA/pF, measured at 0 mV, Cl- equilibrium potential). As the [Mg2+]i increased, the amplitude of IKCa much increased (212±44 pA/pF at [Mg2+]i = 0.5 mM, and 548±92 pA/pF at [Mg2+]i = 2 mM, respectively). The Mg2+effect on the activation of ClCa currents was not distinct. So Vrev of overall caffeine-induced currents shifted to the hyperpolarizing direction as [Mg2+]i increased (-23±7 mV at [Mg2+]i = 0.07 mM, -59±4 mV at [Mg2+]i = 0.5 mM, and -75±1 mV at [Mg2+]i = 2 mM, respectively). In accordance with above results, caffeine evoked membrane depolarization at low [Mg2+]i, but hyperpolarization at high [Mg2+]i. These results suggest that in rabbit CASMCs, KCa and ClCa currents are activated by [Ca2+]i increase. Depending on the relative activity of these two currents, the increased [Ca2+]i can cause either membrane depolarization or hyperpolarization. In determining the direction of feedback regulation of Ca2+, [Mg2+]i plays a crucial role ;supported by BK21 Human Life Sciences and National R & D Project from Ministry of Science & Technology.
Source: Korean Journal of Physiology & Pharmacology.2000 Oct;4(Suppl):S12-S12
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KEYWORD
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Cytosolic Ca2+ not only regulates vascular tone, but also regulates membrane potential by its action on Ca2+-activated ion channels. From this, we can infer the presence of feedback mechanism for regulation of [Ca2+]i in vascular smooth muscle. We investigated the ionic nature of Ca2+-activated currents and modulation of these currents by [Mg2+]i in rabbit coronary arterial smooth muscle cells (CASMCs). Membrane currents were recorded using the whole-cell voltage clamp technique. To induce [Ca2+]i transient, caffeine was briefly applied. At Vhold = -50 mV, caffeine elicited outward or inward currents, and the reversal potential (Vrev) of these currents was in the range from -70 mV to -12 mV. In K+-free condition, however, caffeine elicited only inward current. Vrev of this current was near 0 mV. Replacement of bath Na+ with membrane-impermeable N-methyl D glucamine little affected on the Vrev and amplitude of the inward current. Niflumic acid, a Ca2+-activated Cl- (ClCa) channel blocker suppressed the current. When [Mg2+]i was low (0.1 mM), amplitude of Ca2+-activated K+ current (IKCa) was small (14±6 pA/pF, measured at 0 mV, Cl- equilibrium potential). As the [Mg2+]i increased, the amplitude of IKCa much increased (212±44 pA/pF at [Mg2+]i = 0.5 mM, and 548±92 pA/pF at [Mg2+]i = 2 mM, respectively). The Mg2+effect on the activation of ClCa currents was not distinct. So Vrev of overall caffeine-induced currents shifted to the hyperpolarizing direction as [Mg2+]i increased (-23±7 mV at [Mg2+]i = 0.07 mM, -59±4 mV at [Mg2+]i = 0.5 mM, and -75±1 mV at [Mg2+]i = 2 mM, respectively). In accordance with above results, caffeine evoked membrane depolarization at low [Mg2+]i, but hyperpolarization at high [Mg2+]i. These results suggest that in rabbit CASMCs, KCa and ClCa currents are activated by [Ca2+]i increase. Depending on the relative activity of these two currents, the increased [Ca2+]i can cause either membrane depolarization or hyperpolarization. In determining the direction of feedback regulation of Ca2+, [Mg2+]i plays a crucial role , supported by BK21 Human Life Sciences and National R & D Project from Ministry of Science & Technology.
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