Abstract
Neuropeptide Y has direct vasoconstrictor actions and potentiates the effects of other vasoconstrictor agents. To find out whether both effects of neuropeptide Y are mediated via the same receptor and intracellular mechanism, the interaction between neuropeptide Y and angiotensin II was studied in rabbit femoral arteries. In this preparation, neuropeptide Y, but not its 13–36 fragment, induced constriction. Only neuropeptide Y potentiated the vasoconstrictor response to angiotensin II and the associated rise in inositol-1-phosphate. These potentiating effects of neuropeptide Y were totally prevented by removal of extracellular Ca 2+, partially prevented by a Ca 2+-channel blocker and mimicked by a Ca 2+-channel activator. Pharmacological modulation of adenylate cyclase had no effect. These results suggest that the direct and indirect vascular effects of neuropeptide Y are mediated via Y 1 receptors and depend on the influx of extracellular Ca 2+. The rise in inositol-1-phosphate seems to be secondary to an increase in intracellular Ca 2+, while modulation of adenylate cyclase is apparently not involved.
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