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Am J Physiol Heart Circ Physiol 274: H290-H294, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 1, H290-H294, January 1998

Direct evidence for the role of neuropeptide Y in sympathetic nerve stimulation-induced vasoconstriction

Songping Han, Chun-Lian Yang, Xiaoli Chen, Linda Naes, Bryan F. Cox, and Thomas Westfall

Department of Pharmacological and Physiological Science, Saint Louis University Health Sciences Center, St. Louis, Missouri 63104

Neuropeptide Y (NPY) is a vasoconstrictor peptide and a cotransmitter with norepinephrine (NE) in sympathetic nerve terminals and is thought to be involved in sympathetic nerve stimulation (SNS)-induced vasoconstriction. Using BIBP-3226, a Y1 receptor selective antagonist, we examined this hypothesis in the isolated and perfused mesenteric vascular bed. SNS produced a frequency-dependent increase in perfusion pressure and concomitant overflow of NPY immunoreactivity in the perfusate. [Leu31,Pro34]NPY potentiated NE-induced and ATP-induced vasoconstriction, indicating the presence and biological action of Y1 receptors in this vascular bed. The potentiation effect of [Leu31,Pro34]NPY of the increase in perfusion pressure by NE, ATP, or SNS was prevented by BIBP-3226. In addition, SNS-induced vasoconstriction at both high and low frequencies was significantly attenuated by BIBP-3226 at a concentration that completely blocked the [Leu31,Pro34]NPY-induced potentiation of the NE- or ATP-induced vasoconstrictor effect. These results suggest that ~30% of vasoconstriction produced by SNS depends on NPY in the mesenteric vascular bed.

BIBP-3226; neuropeptide Y release; adenosine 5'-triphosphate; mesenteric vascular bed; rat


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