• 1 January 1982
    • journal article
    • research article
    • Vol. 222  (2) , 338-343
Abstract
The possibility that with some agonists opposing and simultaneously occurring phenomena-contraction-induced increased responsiveness and receptor desensitization in part determine the magnitude of response of the rabbit ear artery was investigated. It has previously been shown that prior contraction of rabbit ear artery by equieffective histamine, KCl or serotonin concentrations increased norepinephrine (NE) responsiveness. The increased NE responsiveness that resulted from prior serotonin-induced contraction was less than that for histamine or KCl. Here, serotonin exposure in the presence of NaNO2 or papaverine concentrations that prevent smooth muscle contraction induced subsequent decreased NE responsiveness. This decreased responsiveness was reversed by KCl in the presence or absence of verapamil, but not by histamine. Ear arteries were everted to separate clearly the 2 phases of agonist-induced contraction. Everted vessels exposed to serotonin in the presence of NaNO2 subsequently responded to NE with initial transient contractions identical to those of controls; the secondary plateau contractions were reduced. Vessels exposed to NE or serotonin in the presence of NaNO2 or papaverine did not induce subsequent decreased norepinephrine and serotonin responsiveness, respectively. Apparently, prior contraction by serotonin induced increased responsiveness which masked underlying .alpha. adrenoceptor desensitization. The desensitization can be reversed by membrane depolarization.