Document Detail


Renal responses to chronic suppression of central sympathetic outflow.
MedLine Citation:
PMID:  22753216     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Chronic electric activation of the carotid baroreflex produces sustained reductions in sympathetic activity and arterial pressure and is currently being evaluated as hypertension therapy for patients with resistant hypertension. However, the chronic changes in renal function associated with natural suppression of sympathetic activity are largely unknown. In normotensive dogs, we investigated the integrative cardiovascular effects of chronic baroreflex activation (2 weeks) alone and in combination with the calcium channel blocker amlodipine, which is commonly used in the treatment of resistant hypertension. During baroreflex activation alone, there were sustained decreases in mean arterial pressure (17±1 mmHg) and plasma (norepinephrine; ≈35%), with no change in plasma renin activity. Despite low pressure, sodium balance was achieved because of decreased tubular reabsorption, because glomerular filtration rate and renal blood flow decreased 10% to 20%. After 2 weeks of amlodipine, arterial pressure was also reduced 17 mmHg, but with substantial increases in norepinephrine and plasma renin activity and no change in glomerular filtration rate. In the presence of amlodipine, baroreflex activation greatly attenuated neurohormonal activation, and pressure decreased even further (by 11±2 mmHg). Moreover, during amlodipine administration, the fall in glomerular filtration rate with baroreflex activation was abolished. These findings suggest that the chronic blood pressure-lowering effects of baroreflex activation are attributed, at least in part, to sustained inhibition of renal sympathetic nerve activity and attendant decreases in sodium reabsorption before the macula densa. Tubuloglomerular feedback constriction of the afferent arterioles may account for reduced glomerular filtration rate, a response abolished by amlodipine, which dilates the preglomerular vasculature.
Authors:
Radu Iliescu; Eric D Irwin; Dimitrios Georgakopoulos; Thomas E Lohmeier
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-07-02
Journal Detail:
Title:  Hypertension     Volume:  60     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-08-16     Completed Date:  2013-01-07     Revised Date:  2013-09-03    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  749-56     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Mississippi Medical Center, 2500 North State St, Jackson, MS 39216-4505, USA.
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MeSH Terms
Descriptor/Qualifier:
Amlodipine / pharmacology
Animals
Baroreflex / drug effects,  physiology*
Blood Pressure / drug effects,  physiology
Calcium Channel Blockers / pharmacology
Carotid Arteries / physiology*
Dogs
Electric Stimulation
Glomerular Filtration Rate / drug effects,  physiology
Kidney / blood supply*,  innervation,  physiology*
Models, Animal
Norepinephrine / blood
Regional Blood Flow / drug effects,  physiology*
Renin / blood
Sodium / metabolism
Sympathetic Nervous System / physiology*
Grant Support
ID/Acronym/Agency:
HL-51971/HL/NHLBI NIH HHS; P01 HL051971/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Calcium Channel Blockers; 51-41-2/Norepinephrine; 7440-23-5/Sodium; 88150-42-9/Amlodipine; EC 3.4.23.15/Renin
Comments/Corrections

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


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