RGD Reference Report - Release of angiotensin-(1-7) from the rat hindlimb: influence of angiotensin-converting enzyme inhibition. - Rat Genome Database

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Release of angiotensin-(1-7) from the rat hindlimb: influence of angiotensin-converting enzyme inhibition.

Authors: Chappell, MC  Gomez, MN  Pirro, NT  Ferrario, CM 
Citation: Chappell MC, etal., Hypertension. 2000 Jan;35(1 Pt 2):348-52.
RGD ID: 1581953
Pubmed: PMID:10642323   (View Abstract at PubMed)

The results of recent studies have demonstrated that angiotensin (Ang)-(1-7) contributes to the antihypertensive actions of either combined ACE/Ang II type 1 receptor blockade or ACE inhibition alone. The vasculature is a key site of action for either drug regimen, and evidence favors a local Ang system within these tissues. Because ACE may degrade Ang-(1-7), we determined whether ACE inhibition alters Ang-(1-7) release from the rat hindlimb perfused with Krebs-Ringer buffer containing Ficoll. Ang-(1-7) release averaged 36+/-13 fmol (period 1, 15-minute collection) and 44+/-11 fmol (period 2) in the control buffer. The addition of the ACE inhibitor lisinopril to the perfusion buffer augmented levels of Ang-(1-7) in periods 3 (144+/-39 fmol) and 4 (163+/-35 fmol; P<0.05 versus 1 or 2, n=8). HPLC and radioimmunoassay of effluent from control or lisinopril treatment demonstrated a single immunoreactive peak with a retention time identical to that of Ang-(1-7). The addition of the neprilysin inhibitor SCH 39370 reduced Ang-(1-7) release in the lisinopril buffer from 177+/-32 (period 1) and 173+/-39 (period 2) fmol to 112+/-24 (period 3) and 87+/-23 fmol (period 4; P<0.05 versus 1 or 2, n=6). Ang I metabolism in the collected perfusate revealed the formation of Ang-(1-7) that was sensitive only to thimet oligopeptidase inhibition; Ang II generation was not detected. The present study demonstrates the recovery of endogenous Ang-(1-7) from the perfused hindlimb. The release of Ang-(1-7) is significantly influenced by inhibition of ACE, which may reflect both increased substrate (Ang I) levels and reduced metabolism of the peptide. Neprilysin inhibition reduced but did not abolish Ang-(1-7) release, which suggests that other endopeptidases may contribute to the release of the peptide.



Gene Ontology Annotations    

Biological Process

Molecular Pathway Annotations    
Objects Annotated

Genes (Rattus norvegicus)
Ace  (angiotensin I converting enzyme)
Mme  (membrane metallo-endopeptidase)


Additional Information