Dopamine increased the slow inward current in the cardiac preparation after blocking (with tetrodotoxin) or eliminating (with Na+-free perfusion) of the 'fast Na+ channel'. Dopamine was, however, ineffective, if the 'slow channel' was blocked (by MnCl2 or D-600) or eliminated (by Ca2+ free perfusion). This adrenaline-like effect of dopamine was prevented by beta-adrenergic blockade (pindolol) and was not modified by previous depletion of tissue catecholamine stores (pretreatment with reserpine). Our data suggest that dopamine affects cardiac electrogenesis through beta-adrenergic receptors and any dopamine-induced noradrenaline release may be only of secondary importance beside this direct agonistic effect.
|Number of pages||7|
|Journal||Polish journal of pharmacology and pharmacy|
|Publication status||Published - Dec 1 1985|
ASJC Scopus subject areas
- Pharmaceutical Science