The distribution of γ‐adrenoceptors and P 2 purinoceptors in mesenteric arteries and veins of the guinea‐pig

1 Membrane potential changes and contractions were recorded from mesenteric arteries and veins of the guinea‐pig, during perivascular nerve stimulation or application of noradrenaline or adenosine triphosphate (ATP). 2 After α‐adrenoceptor blockade, noradrenaline activated low affinity adrenoceptors (γ‐adrenoceptors) causing depolarization and arterial contraction only in the presence of an inhibitor of catecholamine uptake. 3 Noradrenaline did not cause depolarization or contraction of the vein after α‐adrenoceptor blockade even after catecholamine uptake was blocked. 4 Adenosine triphosphate caused depolarization and contraction of both arteries and veins. These responses were abolished by α‐,β‐,methylene adenosine triphosphate (Me‐ATP). 5 Me‐ATP abolished rapid excitatory junction potentials (e.j.ps) caused by perivascular nerve stimulation of arteries but had no effect on arterial responses mediated by γ‐adrenoceptors. 6 In veins, perivascular nerve stimulation evoked slow e.j.ps which persisted in the presence of Me‐ATP but were abolished after blockade of α‐adrenoceptors. 7 The observations indicate that P 2 purinoceptors are present on both mesenteric artery and vein whilst γ‐adrenoceptors are localized near the neuromuscular junction of the artery. However γ‐adrenoceptors do not appear to be directly involved in the generation of arterial e.j.ps.