POTENTIATION OF CARDIOVASCULAR EFFECTS OF CATECHOLAMINES BY A DIPHENYLALKANOLAMINE

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The mechanisms of the CA-potentiating action of DMA, 1-phenyl-l-(2, 5-dimethoxyphenyl)-3-piperidinobutanol, were investigated in cats. DMA specifically prolonged the duration of the cardiovascular responses to adrenaline and isoproterenol. The responses to noradrenaline were only slightly potentiated. While DMA inhibited the disappearance of intravenously injected adrenaline and isopro terenol from blood plasma, the disappearance of noradrenaline was only slightly inhibited. It is suggested that the inhibitory effect of DMA on the disappearance of adrenaline contributed to the potentiating effect of DMA on the pressor response to adrenaline. The increase of the plasma level of <SUP>3</SUP>H-CAs by DMA was not accompanied by any reduction in the total amount of their metabolites. In rabbits, the synergistic effect was observed on the delayed disappearance of plasma <SUP>3</SUP>H-adrenaline among DMA, pyrogallol and tranylcypromine. It is concluded that the DMA-sensitive inactivation process of circulating catecholamines is different from the O-methylation or the monoamine oxidation of catecholamines and has a higher affinity for adrenaline and isoprotcrenol than for noradrenaline.
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