Vasoconstriction after adenosine and inosine in the rat isolated hindlimb abolished by blockade of tryptaminergic mechanisms.

The isolated right hindlimb of the rat was perfused at a fixed flow rate through the femoral artery with heparinized blood from the carotid artery of a donor. Single injections of adenosine (1--300 microgram) induced a biphasic response, a long-lasting vasoconstriction preceded by a transient vasodilatation. Inosine (1--300 microgram) produced only vasoconstriction. After repeated administration of 300 microgram of these substances, the vasoconstriction became less prominent, and finally reverted to vasodilatation. The vasoconstrictor response to these substances (300 microgram) was also diminished or reverted to vasodilatation after pretreatment with reserpine or methysergide. From these results, it is concluded that vasoconstriction after adenosine or inosine may be mediated by 5-hydroxytryptamine released from the peripheral stores and that the intrinsic direct action of these substances on the femoral vascular bed is vasodilator.