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Department of Physiology and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, Louisiana (H.K., L.G.N., A.N.); Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, Tokyo, Japan (M.N.); and Department of Pharmacology and Hypertension and Kidney Disease Research Center, Kagawa University Medical School, Kagawa, Japan (A.N.)
In recent years, the focus of interest on the role of the renin-angiotensin system (RAS) in the pathophysiology of hypertension and organ injury has changed to a major emphasis on the role of the local RAS in specific tissues. In the kidney, all of the RAS components are present and intrarenal angiotensin II (Ang II) is formed by independent multiple mechanisms. Proximal tubular angiotensinogen, collecting duct renin, and tubular angiotensin II type 1 (AT1) receptors are positively augmented by intrarenal Ang II. In addition to the classic RAS pathways, prorenin receptors and chymase are also involved in local Ang II formation in the kidney. Moreover, circulating Ang II is actively internalized into proximal tubular cells by AT1 receptor-dependent mechanisms. Consequently, Ang II is compartmentalized in the renal interstitial fluid and the proximal tubular compartments with much higher concentrations than those existing in the circulation. Recent evidence has also revealed that inappropriate activation of the intrarenal RAS is an important contributor to the pathogenesis of hypertension and renal injury. Thus, it is necessary to understand the mechanisms responsible for independent regulation of the intrarenal RAS. In this review, we will briefly summarize our current understanding of independent regulation of the intrarenal RAS and discuss how inappropriate activation of this system contributes to the development and maintenance of hypertension and renal injury. We will also discuss the impact of antihypertensive agents in preventing the progressive increases in the intrarenal RAS during the development of hypertension and renal injury.
Abstract I. Introduction II. Physiological Actions of Angiotensin II in the Kidney A. Role of Angiotensin II in the Regulation of Renal Hemodynamics B. Role of Angiotensin II in the Regulation of Tubular Function 1. Proximal Tubules. 2. Distal Tubules. 3. Collecting Ducts. III. Regulation of Circulating Renin-Angiotensin System—Classic Renin-Angiotensin System Pathways IV. Mechanisms Responsible for Independent Regulation of Intrarenal Renin-Angiotensin System A. Angiotensinogen B. Renin and Prorenin C. Angiotensin-Converting Enzyme D. Angiotensin II Receptors E. Intrarenal Angiotensin II 1. Interstitial and Tubular Angiotensin II. 2. Intracellular Angiotensin II. F. Alternative Enzyme Pathways G. Other Factors 1. Renal Development and Aging. 2. Gender Differences. V. Augmentation of the Intrarenal Renin-Angiotensin System during Progression of Hypertension and Renal Injury A. Animal Studies 1. Angiotensin II-Dependent Hypertensive Models. a. Angiotensin II-infused hypertensive animals. b. Renovascular hypertensive animals. c. Transgenic animals. 2. Other Hypertensive Models. a. Dahl salt-sensitive rats. b. Spontaneously hypertensive rats. 3. Diabetic Animals. 4. Other Kidney Disease Models. 5. Cardiovascular Implications of Renal-Specific Regulation of the Renin-Angiotensin System. B. Clinical Studies 1. Hypertensive Patients. a. Renovascular hypertension. b. Other hypertension. 2. Patients with Renal Injury. a. Chronic kidney diseases. b. Diabetes. c. Dialysis patients. d. Other kidney diseases. VI. Effects of Pharmacological Intervention with Antihypertensive Agents on the Intrarenal Renin-Angiotensin System A. Angiotensin-Converting Enzyme Inhibitors B. Angiotensin Receptor Blockers C. beta-Blockers D. Calcium Blockers E. Renin Inhibitors and Chymase Inhibitors VII. Conclusions
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