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Hypertension. 2003;41:201-206
Published online before print January 6, 2003, doi: 10.1161/01.HYP.0000049881.25304.73
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(Hypertension. 2003;41:201.)
© 2003 American Heart Association, Inc.


Scientific Contributions

Renoprotection by ACE Inhibition or Aldosterone Blockade Is Blood Pressure–Dependent

Karen A. Griffin; Isam Abu-Amarah; Maria Picken; Anil K. Bidani

From the Departments of Internal Medicine (K.A.G., I.A.-A., A.K.B.) and Pathology (M.P.), Loyola University Medical Center, Maywood, Ill, and Edward Hines Jr Hospital, Hines, Ill.

Correspondence to Karen A. Griffin, MD, Loyola University Medical Center, 2160 South First Ave, Maywood, IL 60153. E-mail Martha.Prado{at}med.va.gov

Renin-angiotensin-aldosterone system blockade has been shown to protect against renal damage in salt-supplemented, stroke-prone spontaneously hypertensive rats (SHRsp). Based on intermittent tail-cuff blood pressure (BP) measurements, it has been claimed that such protection is BP-independent and mediated by a blockade of the direct tissue-damaging effects of angiotensin and/or aldosterone. BP radiotelemetry was performed for 8 weeks in {approx}10-week-old male SHRsp who received a standard diet and either tap water (n=10) or 1% NaCl to drink. Saline-drinking SHRsp were either left untreated (n=12), received enalapril (50 mg/L) in drinking fluid (n=9), or had subcutaneous implantation of time-release 200-mg pellets of aldactone (n=10). The average systolic BP (mean±SEM) during the final 3 weeks was significantly higher (P<0.05) in untreated saline-drinking (215±6 mm Hg) SHRsp but not aldactone-treated (198±4 mm Hg) or enalapril-treated treated SHRsp (173±1 mm Hg), as compared with tap water–drinking SHRsp (197±3 mm Hg). Histological renal damage scores at 8 weeks paralleled the BP in all groups, with an excellent correlation (r=0.8, P<0.001, n=41). Moreover, a renal damage score of >5 was only observed in SHRsp whose average systolic BP during the final 3 weeks exceeded 200 mm Hg, indicating a threshold relation with BP. These data show that protection by renin-angiotensin-aldosterone system blockade in this model is BP-dependent and mediated by preventing the severe increases in BP seen in untreated salt-supplemented SHRsp and further underscore the limitations of interpretations based on conventional tail-cuff BP measurements.


Key Words: hypertension, renal • rats, stroke-prone SHR • nephrosclerosis • autoregulation




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