Résumé
The effects of neuropeptide Y (NPY) on resistance arteries were investigated on 3rd generation mesenteric arterioles of the rat. Contractions were elicited by noradrenaline (NA), 5‐hydroxytryptamine (5‐HT), prostaglandin F 2α (PGF 2α ), depolarization (KCl substituted for NaCl) and by the calcium agonist Bay K 8644, in the absence and in the presence of NPY (100 n m ), a concentration which by itself did not induce vasoconstriction. NPY produced a leftward shift of the concentration‐response curves to the agonists and to KCl, without any alteration of maximal contractions. NPY also potentiated contractions elicited by addition of CaCl 2 to KCl‐depolarized vessels, but its effect on calcium‐induced contractions decreased with increasing KCl concentrations (from 20 to 100 m m ). Calcium‐induced contractions were inhibited by the calcium channel blocker nitrendipine, both in the presence and absence of NPY (100 n m ). NPY increased slightly (but significantly) the sensitivity to nitrendipine (the apparent K B increased from 2.9 × 10 −10 m to 1.6 × 10 −10 m ). The KCl concentration necessary for the maximal effect of Bay K 8644 was decreased in the presence of NPY, and the sensitivity to the calcium channel agonist was increased. Elevating the KCl concentration in the bath from 5 to 20 m m (which gives the same displacement to the left of the KCl concentration‐effect curve seen in the presence of NPY) induced a parallel leftward shift of NA and 5‐HT concentration‐response curves. This shift was identical to the one induced by NPY on 5‐HT‐evoked contractions, but it was significantly smaller ( P < 0.001) than the shift of the NA concentration‐response curve observed in the presence of NPY. In the latter case, NPY enhanced more markedly the contractions induced by low NA concentrations (between 10 −9 and 3 × 10 −8 m ) than those induced by high concentrations (up to 3 × 10 −7 m ), thus giving a shallow concentration‐response curve. The results strongly suggest that NPY partially depolarizes the arterioles and induces an increase in calcium entry through voltage‐dependent channels, thus enhancing contractions elicited by agonists or by KCl‐depolarization. In addition, they support the view that another mechanism also plays a part in the potentiation by NPY of the effects of low concentrations of NA.