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Role of Calcium-activated Potassium Channels in the Genesis of 3,4-diaminopyridine-induced Periodic Contractions in Isolated Canine Coronary Artery Smooth Muscles.

Yasumi Uchida, Yuko Maezawa, Yoshiro Maezawa, Yasuto Uchida, Fumitaka Nakamura

, 2011 Jun 16 , ,

Background: We found that 3,4-diaminopyridine (3,4-DAP), a voltage-gated potassium channel (K(V)) inhibitor, elicits pH-sensitive periodic contractions (PCs) of coronary smooth muscles. Underlying mechanism(s) of PCs however remained to be elucidated. Purpose: The present study was performed to examine the roles of ion channels in the genesis of PCs. Methods: To determine the electromechanical changes of smooth muscles, isolated coronary arterial rings from beagles were suspended in organ chambers filled with Krebs-Henseleit solution and 10(-2) mol/L 3,4-DAP was added to elicit PCs. Results: 3,4-DAP caused periodic spike-and-plateau depolarization accompanied by contraction. PCs were not produced when the CaCl(2) concentration in the chamber was ≤ 0.3×10(-3) or ≥ 10(-2)mol/L. PCs were eliminated by a CaCl(2) concentration ≥ 5×10(-3) mol/L or by lowering pH below 7.20 with HCl and recovered by the addition of iberiotoxin or charybdotoxin which inhibit large-conductance calcium-activated potassium channels (K(Ca)), or by elevating pH above 7.35 with NaOH. PCs, as well as the spike-and-plateau depolarization were eliminated by nifedipine, which inhibits L-type voltage-gated calcium channels (Ca(V)). Conclusions: Influx of Ca(2+) through L-type Ca(V), which was opened because of closing of K(Ca) secondary to 3,4-DAP-induced closing of K(V), resulted in contraction; the intracellular Ca(2+) increased by this influx opened K(Ca), leading to closure of Ca(V) and consequent cessation of Ca(2+) influx, with resultant relaxation; and these processes were repeated spontaneously to cause PCs. H(+) and OH(-) were considered to act opener and closer of K(Ca), respectively.