Document Detail


Renal denervation does not abolish sustained baroreflex-mediated reductions in arterial pressure.
MedLine Citation:
PMID:  17159083     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent studies indicate that suppression of renal sympathetic nerve activity and attendant increments in renal excretory function are sustained baroreflex-mediated responses in hypertensive animals. Given the central role of the kidneys in long-term regulation of arterial pressure, we hypothesized that the chronic blood pressure-lowering effects of the baroreflex are critically dependent on intact renal innervation. This hypothesis was tested in 6 dogs by bilaterally activating the carotid baroreflex electrically for 7 days before and after bilateral renal denervation. Before renal denervation, control values for mean arterial pressure and plasma norepinephrine concentration were 95+/-2 mm Hg and 96+/-12 pg/mL, respectively. During day 1 of baroreflex activation, mean arterial pressure decreased 13+/-1 mm Hg, and there was modest sodium retention. Daily sodium balance was subsequently restored, but reductions in mean arterial pressure were sustained throughout the 7 days of baroreflex activation. Activation of the baroreflex was associated with sustained decreases in plasma norepinephrine concentration ( approximately 50%) and plasma renin activity (30% to 40%). All of the values returned to control levels during a 7-day recovery period. Two weeks after renal denervation, control values for mean arterial pressure, plasma norepinephrine concentration, plasma renin activity, and sodium excretion were comparable to those measured when the renal nerves were intact. Moreover, after renal denervation, all of the responses to activation of the baroreflex were similar to those observed before renal denervation. These findings demonstrate that the presence of the renal nerves is not an obligate requirement for achieving long-term reductions in arterial pressure during prolonged activation of the baroreflex.
Authors:
Thomas E Lohmeier; Drew A Hildebrandt; Terry M Dwyer; Austin M Barrett; Eric D Irwin; Martin A Rossing; Robert S Kieval
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2006-12-11
Journal Detail:
Title:  Hypertension     Volume:  49     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2007 Feb 
Date Detail:
Created Date:  2007-01-19     Completed Date:  2007-02-02     Revised Date:  2007-12-03    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  373-9     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216-4505, USA. tlohmeier@physiology.umsmed.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Baroreflex / physiology*
Blood Pressure / physiology*
Blood Proteins / metabolism
Carotid Arteries / physiology
Denervation
Dogs
Electric Stimulation
Heart Rate / physiology
Hematocrit
Kidney / innervation*,  metabolism
Male
Norepinephrine / blood,  metabolism
Osmolar Concentration
Potassium / blood,  urine
Renin / blood
Sodium / blood,  urine
Sympathetic Nervous System / physiology*
Time Factors
Grant Support
ID/Acronym/Agency:
HL-51971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Blood Proteins; 51-41-2/Norepinephrine; 7440-09-7/Potassium; 7440-23-5/Sodium; EC 3.4.23.15/Renin

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


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