Key result
Ouabain injection evokes reflex coronary vasodilation by activating cholinergic fibers and inhibiting sympathetic fibers.
Ouabain evokes reflex coronary vasodilation by stimulating cardiac receptors, mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.
Ouabain may evoke reflex coronary vasodilation via cardiac receptors in animals; leaves open human relevance and clinical translation.
Experiments were performed to determine the effects of digitalis-induced stimulation of cardiac receptors on the coronary circulation. In chloralose-anesthetized dogs, left circumflex coronary artery was perfused at constant flow, and heart rate was maintained constant by electric pacing. Ouabain injection in the perfused coronary artery produced a significant decrease in coronary perfusion pressure. Epicardial application of lidocaine completely blocked the reflex response. Vagotomy also prevented this reflex response. Sympathetic blockade with intravenous guanethidine or intracoronary phentolamine partially reduced the reflex coronary vasodilatation. Intracoronary atropine also partially reduced the coronary vasodilator response to ouabain. The combined administration of guanethidine and atropine completely abolished the coronary reflex response. These data demonstrate that ouabain can evoke reflex coronary vasodilation by stimulating cardiac receptors. This reflex response is mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.
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Trimarco et al. (1984) studied this question. Ouabain injection was evaluated on Coronary perfusion pressure. Ouabain injection evoked reflex coronary vasodilation by stimulating cardiac receptors, mediated by activating cholinergic vasodilator fibers and inhibiting sympathetic vasoconstrictor fibers.
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