Calcium Independent Contraction of Bladder Smooth Muscle

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