Published online before print October 2, 2006, doi: 10.1161/01.HYP.0000245138.09687.8a
(Hypertension. 2006;48:834.)
© 2006 American Heart Association, Inc.
Editorial Commentaries |
Role of Endothelin Receptors for Renal Protection and Survival in Hypertension
Waiting for Clinical Trials
From the Department of Medicine (M.B.), Internal Medicine I, Medical Policlinic, University Hospital Zürich, Zurich, Switzerland; Molecular Physiology Laboratory (J.J.M., M.A.B.), Centre for Cardiovascular Science, Queens Medical Research Institute, University of Edinburgh, Edinburgh, United Kingdom; and the Division of Nephrology (M.K.), Department of Internal Medicine, University of Michigan, Ann Arbor.
Correspondence to Matthias Barton, University Hospital Zürich, Department of Medicine, Internal Medicine I, Medical Policlinic, Rämistrasse 100, CH-8091 Zürich, Switzerland. E-mail barton@usz.ch
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Hypertension causes mesangial cell growth and glomerulosclerosis and is an important cause of chronic renal failure.1 Urinary loss of proteins is determined by dysfunction of the glomerular filtration barrier for which intact function of visceral glomerular epithelial cells (podocytes) is critical.2,3 Consequently, microalbuminuria and albuminuria have become reliable and early markers of glomerular disease in hypertensive subjects.1,4 In patients, treatment of hypertension with several types of drugs, including angiotensin-converting enzyme inhibitors and angiotensin receptor blockers but also calcium antagonists or ß-blockers, delays the development of renal disease,4 and under certain conditions, proteinuria may actually regress.5 Experimental models of hypertensive renal disease show that established proteinuria and glomerulosclerosis may even be reversed by some drugs.6 However, in the majority of these studies, the drugs also had pronounced antihypertensive effects; thus, pressure-lowering effects of the drugs possibly also contributed to glomerular "healing."7
Mimicking activation of the renin–angiotensin–aldosterone system (RAAS) in rats by infusion of angiotensin II results in hypertension and pronounced vascular hypertrophy8,9; renal and vascular endothelin (ET)-1 synthesis also increases, suggesting an interaction between ET and the RAAS.8,9 This link is further strengthened by studies showing that ETA receptor blockade completely normalizes the structural changes in the vasculature induced by angiotensin II, despite only partially reducing blood pressure.9 Even salt-sensitive hypertension induced by angiotensin II seems to depend on the ET system.10
The interaction between these systems has been investigated further using a genetic model of RAAS-dependent hypertension, a transgenic rat model carrying the mouse renin 2 gene.11 This model
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