Cocaine promotes an apparent direct vasoconstrictor effect of neuropeptide Y in the rat tail artery

Neuropeptide Y is a powerful vasoconstrictor in vivo; however, in vitro it shows weak constrictor effects. This discrepancy may have led to conflicting reports concerning the contractile effects of neuropeptide Y on isolated blood vessels. Using isolated rat tail and femoral artery segments neuropeptide Y (0.1–100 nM) did not induce any contractile response. However, if the catecholamine neuronal uptake blocker cocaine was added to the tissue bath, neuropeptide Y induced a contraction which could be fully blocked by prazosin (1000 nM). Furthermore, an age-dependent increase in the contraction to neuropeptide Y plus cocaine was observed. In conclusion, in the rat tail artery an apparent direct vasoconstrictor effect of neuropeptide Y occurs only in the presence of cocaine. Since this contraction can be fully blocked by prazosin, spontaneously released norepinephrine is an important component of the contraction. The discrepancy between in vivo and in vitro effects of neuropeptide Y may be explained in part by the presence of circulating vasoconstrictors.