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lüll Differential effects of antihypertensive drugs on renal and glomerular hemodynamics and injury in the chronic nitric-oxide-suppressed rat Zhou X; Frohlich EDAm J Nephrol 2005[Mar]; 25 (2): 138-52BACKGROUND/AIMS: Prolonged nitric oxide synthase (NOS) inhibition with N(omega)-nitro-L-arginine methylester in normotensive and hypertensive rats has been demonstrated to produce severe systemic and glomerular hypertension with glomerular sclerosis, and these changes have become a useful experimental model of hypertensive nephrosclerosis. This review summarizes data from our serial studies as well as work of others who are also investigating the effects of the commonly used antihypertensive drugs (including calcium antagonist, angiotensin-converting enzyme inhibitor, angiotensin II type 1 receptor blocker, aldosterone antagonist and thiazide diuretic) on renal and glomerular hemodynamics, renal function and glomerular histopathology using this model. METHODS: A Medline search was performed to identify the relevant literature describing renal effects of antihypertensive drugs in models of hypertension and nephrosclerosis produced or exacerbated by NOS inhibition. RESULTS: Existing data have indicated that most of these drug classes have produced dramatic renoprotective effects, structurally or functionally, on nephrosclerosis induced by prolonged NOS inhibition. CONCLUSION: This review of experimental studies has provided strong evidence supporting the clinical benefits of antihypertensive drugs for hypertensive patients with renal impairment particularly those with endothelial dysfunction associated with NOS deficiency.|Animals[MESH]|Antihypertensive Agents/*pharmacology[MESH]|Endothelium, Vascular/drug effects/physiopathology[MESH]|Hemodynamics[MESH]|Hypertension/complications/physiopathology[MESH]|Kidney Glomerulus/*drug effects/physiopathology[MESH]|Kidney/*drug effects/physiopathology[MESH]|Models, Animal[MESH]|Nephrosclerosis/etiology/physiopathology[MESH]|Nitric Oxide/antagonists & inhibitors[MESH]|Rats[MESH]|Vascular Diseases/complications/physiopathology[MESH] |