Abstract
The effect of 2-(2-pyridyl)ethylamine (PEA) on the rate and force of contraction of cardiac tissues from untreated and reserpine-pretreated guinea-pigs was examined. PEA produced changes in rate of spontaneously beating right atria without activation of H1 or H2-receptors. The positive chronotropic effect of PEA was eliminated when atria from reserpine-pretreated animals were used, indicating an entirely indirect mode of action of PEA in the right atrium. The positive inotropic effect of low doses of PEA in left atria was antagonized by promethazine, whereas the inotropic effect of higher doses of PEA was reduced either by propranolol or following reserpine pretreatment. In the right ventricle strip, the inotropic effect of high doses of PEA was blocked equally by propranolol and promethazine. The results obtained indicate that in the guinea-pig heart, PEA either produces it effects through catecholamine release (right atrium) or through a combination of both H1-receptor stimulation and catecholamine release (left atrium and right ventricle strip). The direct inotropic effects of PEA produced only small increases in force of contraction. The study indicates that caution should be used in ascribing all of the effects of PEA to histamine receptor stimulation.
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