Reserpine-induced postjunctional supersensitivity in rat vas deferens and caudal artery without changes in alpha adrenergic receptors.

Caudal artery and vas deferens from rats treated chronically with reserpine (1 mg/kg/day i.p.) were used to study drug-induced postjunctional supersensitivity in smooth muscle. There was no change in contractile sensitivity of the rat vas deferens after 1 day of reserpine treatment; however, there were similar increases in sensitivity 4 and 7 days after reserpine treatment. The potencies of phenylephrine, methacholine and potassium chloride in causing contraction of the vas deferens were significantly increased by 4.9-, 19.5- and 1.23-fold, respectively, after 7 days of chronic treatment. This treatment also increased the potencies of phenylephrine, serotonin and potassium chloride in causing contraction of rat caudal artery by 1.8-, 1.7- and 1.23-fold, respectively; however, the potency of clonidine was unchanged after 7 days of reserpine treatment. There was no change in sensitivity to phenylephrine 1 day after reserpine treatment but sensitivity was significantly increased after 4 days. There was no significant change in maximum contractile response in either tissue to any of these agents after chronic reserpine treatment. Scatchard analysis of saturation isotherms of specific [125I]BE 2254 binding to membrane fractions from rat vas deferens and caudal artery showed no change in the density or affinity of alpha-1 adrenergic receptors after 1, 4 or 7 days of chronic reserpine treatment. In addition, no change was observed in specific [3H]rauwolscine binding to either tissue after 7 days of chronic reserpine treatment, suggesting no change in alpha-2 adrenergic receptors. These data indicate that changes in alpha adrenergic receptors are not involved in postjunctional supersensitivity of smooth muscle caused by chronic reserpine treatment.