The intrarenal generation of angiotensin II is required for experimental hypertension. (April 2015)

• Record Type: Journal Article
• Authors: Giani, Jorge F; Shah, Kandarp H; Khan, Zakir; Bernstein, Ellen A; Shen, Xiao Z; McDonough, Alicia A; Gonzalez-Villalobos, Romer A; Bernstein, Kenneth E
• Is Part Of: Current opinion in pharmacology. Volume 21(2015)
• Page Start: 73
• Page End: 81
• Publication Date: 2015-04
• Subjects: Pharmacology -- Periodicals; Pharmaceutical Preparations -- Periodicals; Drug Therapy -- Periodicals; Biopharmaceutics -- Periodicals; Pharmacologie -- Périodiques; Pharmacology; Periodicals; 615.105
• DOI: 10.1016/j.coph.2015.01.002
• Languages: English
• ISSNs: 1471-4892

Abstract

Highlights: All components of the RAS are expressed in the kidney. Evidence suggests that the renal RAS functions as a separate entity from systemic RAS. Local generation of angiotensin II by renal ACE is essential for hypertension. Mice lacking renal ACE are protected against hypertension. Abstract : Hypertension is a major risk factor for cardiovascular disease. While the cause of hypertension is multifactorial, renal dysregulation of salt and water excretion is a major factor. All components of the renin–angiotensin system are produced locally in the kidney, suggesting that intrarenal generation of angiotensin II plays a key role in blood pressure regulation. Here, we show that two mouse models lacking renal angiotensin converting enzyme (ACE) are protected against angiotensin II andl -NAME induced hypertension. In response to hypertensive stimuli, mice lacking renal ACE do not produce renal angiotensin II. These studies indicate that the intrarenal renin–angiotensin system works as an entity separate from systemic angiotensin II generation. Renal ACE appears necessary for experimental hypertension.