PT  - JOURNAL ARTICLE
AU  - John Gatgounis
AU  - John Aycock
TI  - EFFECTS OF MONOAMINE OXIDASE INHIBITORS ON ADRENAL MEDULLARY RESPONSES TO NICOTINE AND TETRAMETHYL-AMMONIUM
DP  - 1963 Jul 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 50--57
VI  - 141
IP  - 1
4099  - http://jpet.aspetjournals.org/content/141/1/50.short
4100  - http://jpet.aspetjournals.org/content/141/1/50.full
SO  - J Pharmacol Exp Ther1963 Jul 01; 141
AB  - Intraaortic injection of the MAO inhibitors Ro 5-1025, JB 516, nialamide, iproniazid, isocarboxazid and the non-MAO inhibitor isoniazid in anesthetized dogs with an intact circulatory system produced increments in heart contractile force. Similar injections of iproniazid and nialamide produced decreases in arterial blood pressure while Ro 5-1025, JB 516 and isocarboxazid produced increases in arterial blood pressure. Larger doses of either nialamide (100 mg/kg), iproniazid (200 mg/kg), and isocarboxazid (100 mg/kg) produced decreased cardiac responsiveness to norepinephrine injections. Adrenal medullary responsiveness to nicotine and TMA as judged by autoassay (that is, using contractile force and blood pressure increments as criteria) was significantly blocked by the prior administration of selected doses of these MAO inhibitors. Prior administration of a selected dose of a non-monoamine oxidase inhibitor, isoniazid, and a vehicle did not interfere with chemical stimulation of the adrenal medulla. The relatively slow onset and the prolonged effect of these agents suggest some enzyme activity or chemical change that produces the adrenal blockade. Results of this study tend to indicate that interference with catecholamine release may be a contributing factor in the origin of hypotension following MAO inhibition.