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Partial bladder outlet obstruction abolishes the receptor- and G protein-dependent increase in calcium sensitivity in rabbit bladder smooth muscle

¹Department of Pharmacology and Physiology, Drexel University College of Medicine, Philadelphia 19102; and ²Department of Urology, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104

Submitted 1 April 2004 ; accepted in final form 19 May 2004

Partial bladder outlet obstruction (PBOO) alters the function of the whole bladder and produces specific alterations in the contractility of the bladder smooth muscle cell. The goal of this study was to test the hypothesis that PBOO affects smooth muscle contraction at the level of the receptor- and G protein-dependent increase in myofilament Ca²⁺ sensitivity. To address this question, we used -toxin-permeabilized strips of bladder smooth muscle from control animals and animals subjected to 2 wk of PBOO. Increasing free [Ca²⁺] increased force in permeabilized strips from control animals; the addition of 10 µM carbachol and 10 µM GTP increased both the Ca²⁺ sensitivity of the contractions and the maximal levels of force attained. In contrast, although increases in [Ca²⁺] increased force in permeabilized strips from PBOO animals, the addition of carbachol and GTP had no additional effects. Myosin light chain phosphorylation levels increased with [Ca²⁺], and although they tended to be higher in strips from PBOO animals, they did not reach statistical significance. Assessment of G protein activity from both animal models suggests this is not a site responsible for the loss of carbachol and GTP enhancement of myofilament Ca²⁺ sensitivity. The addition of phorbol dibutyrate increased the Ca²⁺ sensitivity of force development in strips from both animal models, suggesting that an alteration in PKC signaling is not involved. Our results are consistent with the hypothesis that PBOO decreases receptor-mediated myofilament calcium sensitization and that the site of action is downstream from either the G proteins or PKC.

myosin light chain phosphorylation; guanosine 5'-O-(3-thiotriphosphate); protein kinase C; -toxin permeabilization; phorbol dibutyrate

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