Document Detail


Natriuretic and antialdosterone actions of chronic oral NEP inhibition during progressive congestive heart failure.
MedLine Citation:
PMID:  15840018     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Neutral endopeptidase (NEP) degrades atrial natriuretic peptide (ANP) that via cyclic guanosine monophosphate (cGMP) is natriuretic and aldosterone-inhibiting. We hypothesized that chronic oral NEP inhibition (NEPI), initiated in early experimental congestive heart failure (CHF), would delay onset of decreases in sodium excretion during the progression of CHF and, in the severe phase, suppress aldosterone activation and reduce the magnitude of sodium retention. We also hypothesized that chronic NEPI during progressive CHF (PCHF) would improve the natriuretic response to acute volume expansion. METHODS: In a novel canine model that progresses over 38 days from early to moderate and finally severe CHF, we defined the actions of chronic NEPI (candoxatril, 10 mg/kg, orally, twice a day) upon cardiorenal and neurohumoral function as well as the clinical well being of treated and untreated dogs in CHF. RESULTS: From baseline through the moderate phase of CHF, NEPI maintained sodium excretion. In contrast, in moderate CHF, sodium excretion was reduced compared to the early phase in the controls. In severe CHF, sodium excretion was higher with NEPI compared to control. Chronic NEPI also resulted in lower plasma aldosterone as compared to controls. In severe CHF, the natriuretic response to acute saline volume expansion was enhanced with oral NEPI as compared to control. CONCLUSION: This study supports the conclusion that chronic oral NEPI delays the onset of reduction in sodium excretion during the transition from early to severe CHF in this model of PCHF. This therapeutic strategy also improved the natriuretic response to acute volume expansion in severe CHF while enhancing ANP and suppressing aldosterone activation. Thus, these studies demonstrated a selective renal and adrenal action of chronic NEPI in heart failure indicating a therapeutic potential.
Authors:
Fernando L Martin; Tracy L Stevens; Alessandro Cataliotti; John A Schirger; Daniel D Borgeson; Margaret M Redfield; Andreas Luchner; John C Burnett
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Kidney international     Volume:  67     ISSN:  0085-2538     ISO Abbreviation:  Kidney Int.     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-04-20     Completed Date:  2005-08-22     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1723-30     Citation Subset:  IM    
Affiliation:
Cardiorenal Research Laboratory, the Division of Cardiovascular Diseases, Mayo Clinic and Foundation, Rochester, Minnesota 55905, USA. martin.fernando@mayo.edu
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MeSH Terms
Descriptor/Qualifier:
Administration, Oral
Aldosterone / blood
Aldosterone Antagonists / administration & dosage,  pharmacology*
Animals
Atrial Natriuretic Factor / metabolism
Cyclic GMP / metabolism
Disease Models, Animal
Dogs
Heart / drug effects,  physiopathology
Heart Failure / drug therapy*,  physiopathology
Indans / administration & dosage,  pharmacology
Kidney / drug effects,  physiopathology
Male
Natriuresis / drug effects*
Neprilysin / antagonists & inhibitors*
Propionates / administration & dosage,  pharmacology
Protease Inhibitors / administration & dosage,  pharmacology*
Grant Support
ID/Acronym/Agency:
HL-36634/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Aldosterone Antagonists; 0/Indans; 0/Propionates; 0/Protease Inhibitors; 118785-03-8/candoxatril; 52-39-1/Aldosterone; 7665-99-8/Cyclic GMP; 85637-73-6/Atrial Natriuretic Factor; EC 3.4.24.11/Neprilysin

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


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