Abstract

The depressor effect of tryptamine in the chicken was shown to be accompanied by a rise in peripheral resistance and by a rise in right ventricular pressure. The systemic fall in pressure appeared to be the result of an acute pulmonary hypertension. It was not affected by cholinergic blockade with atropine or methylatropine, or by adrenergic blockade with tolazoline or dichloro-isoproterenol, and it was found to be reversed by the MAO inhibitor, tranylcypromine.

That this vasoconstrictor action of tryptamine is not related to cholinergic or adrenergic mechanisms is indicative of the specificity of tryptamine receptors in the chicken cardiovascular system.