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THIRST AND VOLUME, ELECTROLYTE HOMEOSTASIS

Hypertrophy changes the muscarinic receptor subtype mediating bladder contraction from M₃ toward M₂

Temple University School of Medicine, Departments of ¹Urology and ²Pharmacology, Philadelphia, Pennsylvania 19140

Submitted 7 January 2003 ; accepted in final form 16 May 2003

Major pelvic ganglion electrocautery (MPGE) and spinal cord injury in the rat induce bladder hypertrophy and a change in muscarinic receptor subtypes mediating bladder contraction from predominantly M₃ to a combination of M₂ and M₃. To determine whether this is a result of bladder hypertrophy or denervation, we studied the following groups: sham-operated controls, urinary diversion (DIV), MPGE together with urinary diversion (DIV-DEN), bilateral MPGE (DEN), bladder outlet obstruction (BOO), and MPG decentralization (MPGDEC). The degree of bladder denervation was determined by the maximal carbachol response normalized to the response to electric field stimulation. Receptor subtype density was determined by immunoprecipitation. The affinity of subtype-selective muscarinic antagonists for inhibition of carbachol-induced contractions was used to determine the subtype-mediating contraction. DEN, MPG-DEC, and BOO bladders were hypertrophic whereas DIV bladders were atrophic compared with sham operated. Bladder contraction in sham-operated, DIV, and DIV-DEN was mediated by the M₃ receptor subtype, whereas the M₂ subtype participated in contraction in the DEN, MPG-DEC, and BOO groups. The hypertrophied bladders had an increase in total and M₂ receptor density while all experimental groups showed a reduction in M₃ receptor density. Thus bladder hypertrophy, independent from bladder denervation, causes a shift in the muscarinic receptor subtype mediating bladder contraction from M₃ toward M₂.

denervation; outlet obstruction; urinary diversion

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