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Calcium Independent Contraction of Bladder Smooth Muscle
Author(s) -
Yoshimura Yasukuni,
Yamaguchi Osamu
Publication year - 1997
Publication title -
international journal of urology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.172
H-Index - 67
eISSN - 1442-2042
pISSN - 0919-8172
DOI - 10.1111/j.1442-2042.1997.tb00142.x
Subject(s) - medicine , calcium , contraction (grammar) , muscle contraction , smooth muscle , anatomy
Background 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. 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 Ca 2+ ‐free solution containing ethyleneglycol bis (‐aminothylether)‐N,N,‐tetraacetic acid (ECTA), carbachol and phorbol ester produced sustained contractions in detrusor muscle (Ca 2+ ‐free contraction); (2) depletion of Ca 2+ stores by caffeine did not affect Ca 2+ ‐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 Ca 2+ ‐free contraction, while H‐7 (protein kinase C [PKC] inhibitor) abolished this contraction. Conclusions These results suggest that neither stored Ca 2+ 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.