Calcium independent contraction of bladder smooth muscle.

Abstract

Recently, it has been suggested that in vascular smooth muscle a Ca(2+)-independent mechanism or Ca(2+)-sensitization of contractile elements may participate in smooth muscle contraction. In this study, we evaluate this mechanism in detrusor muscle. Strips of smooth muscle from rabbit aorta, rabbit bladder and human bladder were evaluated by in vitro contraction studies. The results show that (1) in Ca(2+)-free solution containing ethyleneglycol bis (-aminothylether)-N,N,-tetraacetic acid (EGTA), carbachol and phorbol ester produced sustained contractions in detrusor muscle (Ca(2+)-free contraction); (2) depletion of Ca2+ stores by caffeine did not affect Ca(2+)-free contraction induced by carbachol; and (3) W-7 (calmodulin inhibitor) and ML-9 (myosin light chain kinase [MLCK] inhibitor) did not show inhibitory effects on Ca(2+)-free contraction, while H-7 (protein kinase C. [PKC] inhibitor) abolished this contraction. These results suggest that neither stored Ca2+ nor the Ca(2+)-calmodulin-MLCK system is involved in the carbachol-induced Ca(2+)-free contraction of detrusor muscle. This Ca(2+)-independent contraction seems to be mediated by the activation of PKC coupled with agonist stimulation of the muscarinic receptor.