The effect of parasympathetic decentralization on the feline urinary bladder.

To examine the pharmacologic nature of parasympathetic decentralization on feline vesical smooth muscle, male cats were subjected to bilateral ventral rhizotomy from levels lumbar 7 to coccygeal 1 and studied at 1 and 3 months. By employing manual bladder decompression twice daily, compensatory bladder hypertrophy was absent or minimal in all specimens. In vitro muscle bath studies of bladder body demonstrated no significant end organ pharmacologic supersensitivity to cholinergic or alpha and beta adrenergic stimulation. Membrane receptor assays displayed a rise in muscarinic cholinergic and beta adrenergic receptors at 1 month which decreased at 3 months. The cholinergic receptor data parallels ultrastructural studies which demonstrate early cholinergic nerve terminal degeneration after motor decentralization followed by subsequent regrowth of cholinergic axons. Alpha 1 and alpha 2 adrenergic receptor densities remained constant in control, 1 month, and 3 month preparations. This lack of classic end organ denervation supersensitivity in the decentralized urinary bladder suggests that other mechanisms may be responsible for eliciting a positive response with the clinical denervation supersensitivity test.