Difference between adrenergic .BETA.1- and .BETA.2-blocking effects on isoproterenol-induced Ca spike suppression in guinea-pig taenia coli.

Publisher Website
Google Scholar
Abstract
Ca spike suppressions induced by isoproterenol (IsP) and a .beta.2-agonist, 5-hydroxymethyl-6-hydroxy-2-isopropylamino-1,2,3,4-tetrahydronaphthalene-1-ol (AA497), were investigated in the presence of butoxamine or practolol. The relaxations were isotonically recorded, and the Ca spike frequency was recorded using the single sucrose gap method. IsP-induced relaxation was not inhibited by butoxamine (Butox, 0.16 .mu.M), but was inhibited by practolol (Prac, 0.188 .mu.M). In 24 mM K+-Krebs'' solution, AA497 caused relaxation in a lower dose range and suppressed to a small extent the Ca spike frequency in a higher dose range, as was observed for IsP-induced curves of log dose-spike frequency and log dose-relaxation. In normal K+-Krebs'' solution, both IsP and AA497 greatly suppressed the Ca spike frequency. IsP (1.21 .mu.M)-induced suppression of the Ca spike frequency was blocked by Prac (113 .mu.M), and it was blocked by Butox (96 .mu.M) to a greater extent. AA497-induced suppression of the spikes was not blocked by Prac (37.6 .mu.M), but completely blocked by Butox (32 .mu.M). These selective inhibitory effects of butoxamine on AA497-induced and IsP-induced Ca spike suppression demonstrate that in the adrenergic .beta.-receptor-mediated process in tenia coli, .beta.2-mechanisms are more closely related to the Ca spike suppression than the .beta.1-mechanisms are.

This publication has 0 references indexed in Scilit: