Abstract

Present study unravels the functional presence of potassium channels and their involvement in mediating beta(2) adrenoceptors-induced myometrial relaxation in buffalo myometrium. Isolated myometrial preparations exhibited rhythmic spontaneity with regular pattern of amplitude and frequency. Levcromakalim produced concentration-dependent inhibitory effect on myometrial spontaneity and relaxant effect and the dose-response curve (DRC) was shifted towards right in the presence of glybenclamaide. In the tissues pretreated with glybenclamide, relaxant effect of albuterol was significantly (P < 0.05-0.001) lower (pD(2) = 6.94, R(max) = 96.8 +/- 3.3%; n = 5) compared with albuterol alone (pD(2) = 8.55, R(max) = 101.1 +/- 6.3%; n = 6) and the DRC was shifted to right. In the presence of tetraethyl ammonium (TEA) also, significant (P < 0.001) rightward shift of DRC of albuterol with decrease in maximal effect (pD(2) = 8.05, R(max) = 71.2 +/- 7.4%; n = 7 vs. control pD(2) = 8.55, R(max) = 101.1 +/- 6.3%; n = 6) was observed. On the other hand, 4-aminopyridine (1 mm) sensitized the myometrial strips and increased the amplitude and frequency/min of myometrial spontaneity but failed to significantly alter the DRC of albuterol. Results of present study suggest the functional presence of K(ATP), BK(Ca) and K(V) channels in buffalo myometrium, but beta(2)-adrenoreceptor agonist-induced myometrial relaxation seems to be K(ATP) and BK(Ca) channel-dependent only. Further, our studies also suggest promising therapeutic potential of potassium channel modulators as tocolytics in buffaloes.

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