The activation of Ca2+-dependent K+ conductance by adrenaline in mouse peritoneal macrophages |
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Authors: | N Hara M Ichinose M Sawada T Maeno |
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Institution: | (1) Department of Physiology, Shimane Medical University, 693 Izumo, Japan;(2) Central Research Laboratories, Shimane Medical University, 693 Izumo, Japan |
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Abstract: | Responses to adrenaline in mouse peritoneal macrophages were investigated with perforated and cell-attached patch-clamp recording, and with a combination of the perforated-patch recording and fura-2 fluorescence measurements. Extracellularly applied adrenaline induced a transient outward current (4–10s in duration, 100–500 pA in amplitude) at –40 mV associated with a marked increase in conductance. The adrenaline-induced current I
o (Adr)] reversed polarity near –80 mV. The reversal potential depended distinctly on the external K+ concentration but not on external Cl– concentration. Removal of external Ca2+ did not affect I
o(Adr) within 2–4 min but subsequent responses to adrenaline were progressively depressed. In contrast, treatment with an intracellular Ca2+ chelator, the acetoxymethyl ester of 1,2-bis-(2-aminophenoxy)ethane-N,N,N,N-tetraacetic acid completely abolished I
o(Adr). Furthermore, I
o(Adr) was blocked by bath-applied quinidine and charybdotoxin, but not by tetraethylammonium or apamin. Extracellular application of an
1-adrenoceptor agonist phenylephrine and of noradrenaline mimicked I
o(Adr). On the other hand, I
o(Adr) was antagonized by a non-selective -adrenoceptor antagonist phentolamine (0.2 M) and an
1-adrenoceptor antagonist prazosin (0.2 M), but was not affected by an 2-adrenoceptor antagonist yohimbine (1 M) or a -adrenoceptor antagonist propranolol (1 M). Cell-attached single-channel recordings with the pipette solution containing 145 mM KCl revealed the activation of single-channel currents with a conductance of 40 pS during application of adrenaline outside the patch. Parallel measurements of membrane current and fura-2 fluorescence in the same cell demonstrated a correlation between the rise in Ca2+]i and an increase in K+ conductance. Therefore, it is concluded that adrenaline activates a Ca2+-dependent K+ conductance by release of Ca2+ from internal stores through an activation of an
1-adrenoceptor. |
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Keywords: | Adrenaline
1-Adrenoceptor" target="_blank">gif" alt="agr" align="BASELINE" BORDER="0">
1-Adrenoceptor Ca2+ release Ca2+-dependent K+ conductance Patch clamp Mouse peritoneal macrophage |
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