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 alpha-adrenoceptor blockade, noradrenaline activated low affinity adrenoceptors (gamma-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 alpha-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 alpha-,beta-,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 gamma-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 alpha-adrenoceptors. 7. The observations indicate that P2 purinoceptors are present on both mesenteric artery and vein whilst gamma-adrenoceptors are localized near the neuromuscular junction of the artery. However gamma-adrenoceptors do not appear to be directly involved in the generation of arterial e.j.ps.
