title: Impact of angiotensin II on the kidney: does an angiotensin II receptor blocker make sense?
abstract: The renin-angiotensin system (RAS) regulates blood pressure, volume, and electrolyte balance. Derangements of the RAS may contribute to hypertension and renal injury, particularly in patients with types 1 or 2 diabetes. Angiotensin-converting enzyme (ACE) inhibitors have been proven to be beneficial in patients with hypertension and diabetes by preventing or delaying the development and progression of proteinuria and glomerulosclerosis. Comparisons with other drug classes demonstrate renoprotective effects for ACE inhibitors that are independent of-and additive to-their systemic antihypertensive actions. These renal effects may derive from their preferential dilation of renal efferent arterioles, which further reduces intraglomerular pressure. Inhibition of angiotensin II (Ang II) synthesis is subtotal, however, because local non-ACE enzymes also convert Ang I to Ang II. The existence of alternative pathways for Ang II generation that are unaffected by ACE inhibitors raises questions about whether ACE is the optimal target for RAS suppression. Ang II receptor blockers (ARBs), which interrupt the RAS at the target-organ receptor level, will block the effect of angiotensin whether its production involved ACE or a non-ACE pathway. ARBs are currently undergoing clinical trials to assess their efficacy in hypertensive patients with nephropathy.
authors.affiliation: Radiology Department, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA. djpagecapo@rics.bwh.harvard.edu
authors.forename: N K
authors.initials: NK
authors.lastname: Hollenberg
mesh_terms: D000804:Angiotensin II / Q000037:antagonists & inhibitors / Q000502:physiology*; D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D001810:Blood Volume / Q000187:drug effects / Q000502:physiology; D002986:Clinical Trials as Topic; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000503:physiopathology; D018450:Disease Progression; D005923:Glomerulosclerosis, Focal Segmental / Q000517:prevention & control; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000502:physiology*; D007703:Peptidyl-Dipeptidase A / Q000187:drug effects / Q000502:physiology; D011507:Proteinuria / Q000517:prevention & control; D012084:Renin-Angiotensin System / Q000187:drug effects / Q000502:physiology; D014665:Vasodilator Agents / Q000627:therapeutic use; D014882:Water-Electrolyte Balance / Q000187:drug effects / Q000502:physiology
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D007703:Peptidyl-Dipeptidase A