Abstract
Neuropeptide Y (NPY) has been shown to potentiate the response of the isolated rabbit ear artery to field stimulation, provided that the vascular endothelium is intact. This report describes efforts to elucidate the mechanism by which NPY produces this effect. The response of the perfused rabbit ear artery to brief intermittent field stimulation was significantly enhanced by NPY (100 nmol/L). The administration of indomethacin (10 mumol/L) to inhibit cyclooxygenase did not affect the ability of NPY to potentiate neurogenic vasoconstriction. Blockade of calcium channels with nifedipine (1 mumol/L) produced a partial attenuation of the NPY effect. Our studies therefore suggest that an arachidonic acid metabolite is not involved in NPY induced potentiation of vascular neuroeffector transmission in the rabbit ear artery. On the other hand, the translocation of extracellular calcium may play a role in this process.
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