This Article Free Full Text (Free PDF) Free References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Stevanovic, R. D Articles by Hollenberg, N. K Search for Related Content PubMed PubMed Citation Articles by Stevanovic, R. D Articles by Hollenberg, N. K Social Bookmarking                         What's this?

Renin Release in Response to Renin System Blockade: Activation of the Renin System in Type 1 Diabetes Mellitus

Departments of Medicine and Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA, rachko{at}aol.com

Deborah A Price

Departments of Medicine and Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

M Cecilia Lansang

Departments of Medicine and Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

Naomi DL Fisher

Departments of Medicine and Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

Lori MB Laffel

Joslin Diabetes Center, Harvard School of Medicine, Boston, Massachusetts, USA

Norman K Hollenberg

Departments of Medicine and Radiology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA

Activation of the renin-angiotensin system (RAS) in diabetes is thought to contribute to nephropathy. This is suggested by findings of an enhanced renovascular (RPF) response to RAS blockade with angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin receptor blockers (ARBs). An alternative approach to assess RAS activation is the evaluation of renin release following RAS blockade.

Forty-four consecutively enrolled Type 1 diabetic patients (28.2 ± 1.5 years) and 37 normal subjects (37 ± 2.6 years) in high salt balance were given 25 mg of captopril and 16 mg of candesartan p.o. on consecutive days. All subjects were Caucasian. All, except one diabetic patient, had normal renal function. Plasma renin activity (PRA) and renal plasma flow (RPF) were measured for four hours after both drugs, and at eight, and 24 hours after candesartan.

As anticipated, both drugs increased PRA. Peak responses (90' after captopril) were 5.6 ± 1 ng/mL Ang I/hour in diabetic patients, and 1.7 ± 0.9 ng/mL Ang I/hour in normal subjects (p<0.001). Responses to both drugs were correlated in diabetic patients for PRA (r=0.623; p=0.001) and for RPF (r=0.9; p<0.001). When the PRA response to captopril was below the median, the RPF response was limited (22.1 ± 17.6 ml/minute/1.73 m²). When it was above the median, the RPF response was also larger (62.2 ± 13.9 ml/minute/1.73 m²; p=0.006).

Renin response to ACE-I and ARB confirms activation of the RAS in diabetic patients.

Key Words: Diabetes • Renin • Renal plasma flow

Journal of Renin-Angiotensin-Aldosterone System, Vol. 6, No. 2, 78-83 (2005)
DOI: 10.3317/jraas.2005.013


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?