Document Detail

Dynamic exercise attenuates spontaneous baroreceptor reflex sensitivity in conscious rats.
MedLine Citation:
PMID:  12861339     Owner:  NLM     Status:  MEDLINE    
In humans, it has been reported that dynamic exercise attenuates spontaneous baroreceptor reflex sensitivity (sBRS), which is an index of the gain of the baroreceptor-cardiac reflex. We demonstrated previously that endogenously produced NO from endothelial nitric oxide synthase (eNOS) within the nucleus tractus solitarii (NTS), the central terminal site of baroreceptor afferents, depressed sBRS. In this study, we investigated whether eNOS activity within the NTS plays any role in down-modulating the sBRS during dynamic exercise. In conscious Wistar rats arterial pressure and heart rate (HR) were monitored continuously and chronically using radiotelemetry before and during wheel cage running at 6 m min(-1) for 10 min. sBRS was determined by a time-series method. During dynamic exercise systolic blood pressure (SBP) and HR were significantly increased (SBP: 138 +/- 2 vs. 125 +/- 2 mmHg, P < 0.001; HR: 447 +/- 6 vs. 362 +/- 8 beats min(-1), P < 0.001) while sBRS was significantly decreased (0.53 +/- 0.03 vs. 1.08 +/- 0.08 ms mmHg(-1), P < 0.001). In sino-aortic denervated rats the change in SBP in response to dynamic exercise was significantly larger than that in baroreceptor-intact rats (denervated: 21.6 +/- 2.5 mmHg; intact: 12.0 +/- 2.8 mmHg, P < 0.05). In contrast, denervation made no difference to the change in HR. Although disabling eNOS activity in the NTS by adenoviral-directed expression of a dominant negative mutant form of eNOS increased resting sBRS (1.48 +/- 0.20 vs. 1.09 +/- 0.15 ms mmHg(-1), P < 0.05), the absolute level reached during dynamic exercise was identical to control. These results demonstrate that during dynamic exercise (i) the sBRS decreases around the operating point of the baroreceptor-cardiac reflex function curve in normotensive rats, (ii) the baroreceptor reflex operates to limit the rise in arterial pressure, and (iii) the attenuation of sBRS is not mediated by changes in eNOS activity within the NTS.
Hidefumi Waki; Sergey Kasparov; Kiyoaki Katahira; Tsuyoshi Shimizu; David Murphy; Julian F R Paton
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Experimental physiology     Volume:  88     ISSN:  0958-0670     ISO Abbreviation:  Exp. Physiol.     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-07-15     Completed Date:  2004-09-16     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  9002940     Medline TA:  Exp Physiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  517-26     Citation Subset:  IM    
Department of Physiology, School of Medical Sciences, University of Bristol, Bristol BS8 1TD, UK.
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MeSH Terms
Adenoviridae / genetics
Aorta / innervation,  physiology
Baroreflex / physiology*
Blood Pressure / physiology
Heart Rate / physiology
Nitric Oxide Synthase / antagonists & inhibitors,  genetics,  metabolism
Nitric Oxide Synthase Type III
Physical Exertion / physiology*
Rats, Wistar
Reg. No./Substance:
EC Oxide Synthase; EC Oxide Synthase Type III; EC protein, rat

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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