Inhibition of cardiac sympathetic neurotransmission by histamine in the dog is mediated by H1‐receptors

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Abstract
1 The role of histamine H1- and H2-receptors in mediating prejunctional inhibition of cardiac sympathetic neurotransmission and histamine-induced coronary vasodilatation were investigated in perfused dog hearts in situ. 2 Intra-arterial injections of histamine into the right coronary artery during the resting state caused slightly positive chronotropic responses in doses larger than 1 μg. 3 Histamine in doses of 0.1 to 10 μg into the right coronary artery reduced the tachycardia resulting from electrical stimulation of the cardiac sympathetic nerves. 4 Intra-coronary infusions of chlorpheniramine (300 μg/min) significantly reduced the histamine-induced depression of cardiac nerve stimulation. The effects of cimetidine (300 μg/min) and metiamide (300 μg/min) were less pronounced. 5 Histamine (1 to 10 μg) further increased heart rate resulting from the continuous intra-coronary infusion of noradrenaline (1 or 3 μg/min). 6 Intra-arterial injections of histamine (0.1 to 10 μg) caused an increase in coronary blood flow in a dose-dependent manner. This was partially inhibited by intra-coronary infusion of chlorpheniramine (10 to 300 μg/min) and by cimetidine (10 to 300 μg/min). The combination of both drugs (10 to 100 μg/min of each) caused a larger inhibition. 7 The present results suggest that the histamine-induced depression of heart rate during cardiac sympathetic nerve stimulation is due to a prejunctional effect mediated mainly by H1-receptors. Histamine-induced coronary vasodilatation in the dog is mediated both by H1- and H2-receptors.