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Articles in PresS, published online ahead of print July 18, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00827.2001
Submitted on September 24, 2001
Accepted on July 12, 2002
1 Internal Medicine, University of California, Davis, Davis, CA, USA
2 Human Physiology, University of Newcastle, Callaghan, Callaghan, NSW, Australia
3 Internal Medicine, University of California, Davis, Davis, CA, USA; Pharmacology, University of California, Davis, Davis, CA, USA
* To whom correspondence should be addressed. E-mail: cych{at}ucdavis.edu.
In hypertensive subjects a single bout of dynamic exercise results in an immediate lowering of blood pressure back towards normal. This post-exercise hypotension (PEH) also occurs in the spontaneously hypertensive rat (SHR). In both humans and SHRs, PEH features a decrease in sympathetic nerve discharge, suggesting the involvement of CNS pathways. Given that substance P is released in the nucleus tractus solitarius (NTS) by activation of baroreceptor and skeletal muscle afferent fibers during muscle contraction, we hypothesized that substance P acting at neurokinin 1 (NK1) receptors in the NTS might contribute to PEH. We tested the hypothesis by determining, in conscious SHRs, whether NTS microinjections of the NK1 receptor antagonist, SR-140333, before exercise attenuated PEH. The antagonist, in a dose (60 pmole) that had no effect on blood pressure before or during exercise but that blocked substance P- and spared DL-homocysteic acid-induced depressor responses, significantly attenuated the PEH by 37%. Vehicle microinjection had no effect. The antagonist also had no effect on heart rate responses both during exercise and PEH period. The data suggest that a substance P (NK1) receptor mechanism in the NTS contributes to PEH.
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