Abstract
Neuropeptide Y (NPY) is a potent pressor agent that is stored in the sympathetic nerves. In several species, NPY release is augmented when sympathetic impulse frequencies increase. We investigated the extent to which NPY contributes to the pressor response to high- and low-frequency electrical stimulation. Rats were pithed, and the sympathetic trunk was stimulated at either 20 or 3 Hz in the presence or absence of antagonists of NPY and alpha andbeta adrenergic receptors. The 20-Hz stimulation raised plasma NPY levels, but the 3-Hz stimulation did not. The 20-Hz stimulation caused marked pressor responses that were maintained for several minutes after the end of stimulation regardless of whether rats were pretreated with adrenergic blockers. The NPY antagonists BIBP 3226 and 1229U91 reduced the size of the pressor response that followed 20 Hz stimulation by >50%. The rapid blood pressure spikes that occur during electrical stimulation are attenuated by alphaadrenergic but not by NPY antagonists. There is a prolonged pressor response after high-frequency stimulation of the sympathetic trunk in pithed rats that begins after 1 to 2 min of stimulation and lasts ∼10 min after the end of stimulation. At least half of this pressor response is mediated by NPY.
Footnotes
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Send reprint requests to: Dr. Brian Kennedy, Department of Medicine, University of California, San Diego Medical Center, 200 W. Arbor Drive, San Diego, CA 92103-8341.
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↵1 This work was supported by National Institutes of Health Grants HL35924 and RR00827.
- Abbreviations:
- NPY
- neuropeptide Y
- NE
- norepinephrine
- BP
- blood pressure
- MIPR
- mean integrated pressor response
- MAP
- mean arterial pressure
- ANOVA
- analysis of variance
- Received May 17, 1996.
- Accepted December 23, 1996.
- The American Society for Pharmacology and Experimental Therapeutics
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