Abstract

Potassium ( 42K) or chloride ( 36Cl) efflux curves were determined in guinea-pig vas deferens from control, reserpine-treated animals (1 mg/kg/day i.p. for 5 days), and from animals whose vas deferens had been sympathetically denervated 1 week before. Steady-state 42K turnover in control tissues was 0.0052 ± 0.0002 min −1; neither reserpine treatment nor sympathetic denervation changed this parameter significantly. Control 36Cl turnover was 0.058 ± 0.002 min −1 and it was unaffected by either procedure. Methoxamine (3 × 10 −6 to 10 −4 M) induced dose-related increases in the fractional exchange of 42K and 36Cl. These were of greater magnitude after sympathetic denervation or reserpine treatment. Furtrethonium also produced dose-dependent increases in 42K efflux; its dose-response curve was shifted 2.6-fold to the left of the control curve by reserpine treatment. These results indicate that interruption of adrenergic transmission to the guinea-pig vas deferens is associated with increased changes in membrane permeability to Cl and possibly K in response to drug activation of α-adrenergic and cholinegic receptors. It is suggested that the supersensitivity phenomenon observed in the guinea-pig vas deferens after reserpine or sympathetic denervation is, in part, related to improved transduction of drug-receptor interaction into ionic permeability changes.

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