Mechanisms for inhibitory action of ethanol on contraction of rat bladder smooth muscle – Analysis using rat bladder smooth muscle cells in primary culture – *
Mechanisms for the inhibitory action of ethanol on urinary bladder smooth muscle were investigated using bladder smooth muscle strips and smooth muscle cells in primary culture. KC1 (126 mM) -induced contraction of the smooth muscle strips was dose-dependently inhibited by ethanol and verapamil, an inhibitor specific to L-type voltage-dependent Ca2+channels (VDCCs), and simultaneous addition of these two agents had neither additive nor synergic effects on the KC1-induced contraction. KC1 increased [45Ca2+] influx into rat bladder muscle cells in a dose-dependent manner with maximal stimulation at 50 mM. This stimulatory effect of 50 mM KC1 was dose-dependently suppressed by tetrodotoxin, a membrane depolarization inhibitor, and membrane-stabilizing drugs such as dibucaine and procainamide. The influx was completely abolished when these drugs showed their maximal effects. These results indicate that the KC1-evoked [45Ca2+] influx into bladder smooth muscle cells is mediated via activation of L-type VDCCs subsequent to membrane depolarization. Ethanol also reduced the KC1-induced [45Ca2+] influx in a dose-dependent manner to the basal level of influx. In addition, [45Ca2+] influx induced by Bay k 8644, an activator of L-type VDCCs, was completely suppressed by ethanol. These results indicate that ethanol induced relaxation of bladder smooth muscle via its inhibitory action on Ca2+ entry into smooth muscle cells which was induced by activation of L-type VDCCs. (Accepted on May 24, 1999) Kawasaki Igakkaishi 25(2) : 77―86, 1999
