| Region-specific changes in sympathetic nerve activity in angiotensin II-salt hypertension in the rat. | |
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MedLine Citation:
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PMID: 19717492 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It is now well accepted that many forms of experimental hypertension and human essential hypertension are caused by increased activity of the sympathetic nervous system. However, the role of region-specific changes in sympathetic nerve activity (SNA) in the pathogenesis of hypertension has been difficult to determine because methods for chronic measurement of SNA in conscious animals have not been available. We have recently combined indirect, and continuous and chronic direct, assessment of region-specific SNA to characterize hypertension produced by administration of angiotensin II (Ang II) to rats consuming a high-salt diet (Ang II-salt hypertension). Angiotensin II increases whole-body noradrenaline (NA) spillover and depressor responses to ganglionic blockade in rats consuming a high-salt diet, but not in rats on a normal-salt diet. Despite this evidence for increased 'whole-body SNA' in Ang II-salt hypertensive rats, renal SNA is decreased in this model and renal denervation does not attenuate the steady-state level of arterial pressure. In addition, neither lumbar SNA, which largely targets skeletal muscle, nor hindlimb NA spillover is changed from control levels in Ang II-salt hypertensive rats. However, surgical denervation of the splanchnic vascular bed attenuates/abolishes the increase in arterial pressure and total peripheral resistance, as well as the decrease in vascular capacitance, observed in Ang II-salt hypertensive rats. We hypothesize that the 'sympathetic signature' of Ang II-salt hypertension is characterized by increased splanchnic SNA, no change in skeletal muscle SNA and decreased renal SNA, and this sympathetic signature creates unique haemodynamic changes capable of producing sustained hypertension. |
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Authors:
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John W Osborn; Gregory D Fink |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2009-08-28 |
Journal Detail:
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Title: Experimental physiology Volume: 95 ISSN: 1469-445X ISO Abbreviation: Exp. Physiol. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-01-12 Completed Date: 2010-08-04 Revised Date: 2010-09-27 |
Medline Journal Info:
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Nlm Unique ID: 9002940 Medline TA: Exp Physiol Country: England |
Other Details:
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Languages: eng Pagination: 61-8 Citation Subset: IM |
Affiliation:
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Department of Integrative Biology and Physiology, University of Minnesota, Room 6-125 Jackson Hall, Minneapolis, MN 55455, USA. osbor003@umn.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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physiology* Animals Disease Models, Animal* Humans Hypertension / etiology, metabolism*, physiopathology* Kidney / innervation Muscle, Skeletal / innervation Rats Sodium Chloride, Dietary / adverse effects* Sympathetic Nervous System / physiology* Viscera / innervation |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL076312-05/HL/NHLBI NIH HHS; R01HL076312/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Sodium Chloride, Dietary; 11128-99-7/Angiotensin II |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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