THE DEPLETION OF CATECHOLAMINE OF THE RABBIT’S ATRIA BY RESERPlNE IN VITRO

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Abstract
The actions of reserpine, iproniazid, and trans-2-phenylcyclopropylamine (SKF 385) in vitro on the norepinephrine content in rabbit''s atria have been studied in this experiment. The estimation of norepinephrine was followed to the method introduced by Carlsson. The mean content of norepinephrine was 1.48 [plus or minus] 0.11 [mu]g/g for the right atrium and 0.93 0.12 [mu]g/g for the left atrium. The right atrium always contained larger amounts of norepinephrine than the left atrium. Reserpine slightly released heart norepinephrine in vitro in the doses which abolished both the rhythmic contraction of the atrial preparation and the transmembrane potential of the pacemaker and atrial non-pacemaker fibers within 2 hours after the administration. The depletion of norepinephrine was larger in the right atrium (20%) than in the left atrium (15%). But the depletion of norepinephrine in vitro was much smaller than in vivo. Monoamine oxidase inhibitors, iproniazid and SKF 385, blocked the spontaneous release of norepinephrine of atria, and at 2 1/2 hours after the administration of iproniazid the norepinephrine content was 1.46 [plus or minus] 0.22 [mu]g/g for the right atrium and 0.81 [plus or minus] 0.12 Mg/g for the left. In the case of SKF 385 the norepinephrine content was 1.52 [plus or minus] 0.13 [mu]g/g for the right atrium and 0.84 [plus or minus] 0.04 [mu]g/g for the left. Pretreatment with iproniazid or SKF 385 reversed the action of reserpine, and increased the amount of norepinephrine in the atria. The increase of norepinephrine was usually much larger in the right atrium than in the left atrium. It was expected that the depressive effect of reserpine on the rhythmic contraction of the extirpated rabbit''s atrial preparation might have some relation with the depletion of the catecholamine. However, the results in this experiment did not completely clarify the depressive effect of reserpine and some mechanism of reserpine other than the depletion of catecholamine should be required to explain the complete abolition of spontaneous contraction of the atria.

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