Tryptaminergic mechanism participating in induction of vasoconstriction by adenine nucleotides, adenosine, IMP and inosine in the isolated and blood-perfused hindlimb preparation of the rat.

The isolated right hindlimb of the recipient rat was perfused at a constant flow rate through the femoral artery with heparinized blood from the carotid artery of a donor. The preparations were under a 99.0 +/- 0.8 mmHg of mean perfusion pressure (N = 63) and 3.3 +/- 0.1 ml/min of blood flow through the right femoral artery. The actions of adenosine, adenosine tri-, die- and monophosphate, inosine monophosphate and inosine on the femoral vascular bed were investigated, respectively. These substances injected into the femoral artery, with the exception of inosine, caused a dose-dependent vasoconstriction always preceded by a temporal vasodilatation. Inosine induced only a prompt vasoconstriction. The vasoconstrictor responses to these substances were diminished or reverted to vasodilator ones after repeated administrations and such were significantly prevented by pretreatment with either reserpine or methysergide. These results indicate that all the purines tested induce a vasoconstriction in the femoral vascular bed of the rat through a common (tryptaminergic) mechanism and that such seem to be potent releasers of 5-hydroxytryptamine from peripheral tryptaminergic storage sites.