POSITIVE INOTROPIC EFFECT OF NICOTINE ON ELECTRICALLY EVOKED CONTRACTION OF ISOLATED TOAD VENTRICLE

  • 1 January 1984
    • journal article
    • research article
    • Vol. 267  (2) , 269-278
Abstract
The mechanism of the responses of nicotine on electrically evoked contractions of the isolated spirally cut toad ventricle was investigated. Nicotine produced a concentration-dependent positive inotropic effect of the ventricle. Prior administration of propranolol, hexamethonium, hemicholinium-3 or guanethidine failed to antagonize the positive inotropic effect of nicotine, thus ruling out the possibility of the nicotine effect being mediated through activation of .beta.-adrenoceptors, ganglionic activation, presynaptic liberation of acetylcholine and liberation of norepinephrine from the sympathetic nerve endings, respectively. The positive inotropic effect is probably mediated through mobilization of Ca since prior incubation with verapamil, the Ca transport blocker, and EDTA, which chelates the extracellular Ca and Ca-free Ringer, prevented the positive inotropic effect of nicotine. The positive inotropic effect of nitocine may be due to the facilitating effects of nicotine on Ca2+ exchange or mobilization of membrane bound Ca2+.