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  • Title: Adrenaline-induced amplification of sympathetic activity during rest and stress: inhibition by non-selective and beta 1-selective beta-adrenoceptor blockade.
    Author: van den Meiracker AH, Man in't Veld AJ, Boomsma F, Blankestijn PJ, Schalekamp MA.
    Journal: J Hypertens Suppl; 1988 Dec; 6(4):S558-61. PubMed ID: 2907349.
    Abstract:
    In a placebo-controlled randomized cross-over trial the effects of non-selective (bopindolol, 1 mg once daily for 1 week) and of beta 1-selective beta-adrenoceptor blockade (atenolol, 50 mg once daily for 1 week) on adrenaline-induced enhancement of basal and stimulated sympathetic activity were studied in 10 hypertensive subjects. During infusion of adrenaline (20 ng/kg per min) venous plasma adrenaline levels increased into the high physiological range. Resting concentrations of arterial plasma noradrenaline and of the basal production of noradrenaline in the forearm increased significantly (P less than 0.01) during infusion of adrenaline. The increases in these two indices of sympathetic activity were abolished by bopindolol and by atenolol. Arterial noradrenaline, but not noradrenaline production, also increased in response to isometric exercise, cold provocation and mental stress during infusion of adrenaline (P less than 0.05). These amplifications were also abolished by both beta-adrenoceptor antagonists. Our findings provide further evidence in man for a stimulatory effect of adrenaline in the physiological range on sympathetic activity. This effect, which is supposed to be mediated by prejunctional beta-adrenoceptors, can be blocked not only by non-selective, but also by beta 1-selective beta-adrenoceptor antagonists.
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