Treatment of hypertension in renal disease.
Experimental and clinical evidence are summarized that support the hypothesis that enhanced transmission of systemic hypertension to the adapted glomerulus in the setting of reduced nephron mass may be responsible for accelerated vascular and glomerular damage in the hypertensive stage of parenchymal renal disease in man. In experimental models of hypertension associated with reduced renal mass, the kidney appears to be damaged directly by transmission of pressure rather than primarily through vasoconstriction and ischemia. When hypertension is combined with models of glomerular disease, vascular and glomerular injury are aggravated. It is proposed that adaptive glomerular hemodynamic alterations which occur in parenchymal renal disease magnify the transmission of increased pressure and flows when hypertension supervenes. Accelerated vascular and glomerular damage and functional deterioration result. According to this hypothesis, control of systemic hypertension and minimization of hydraulic stress on the diseased glomerulus become critical to the management of chronic renal disease and the prevention of progressive renal insufficiency.
D000818:Animals; D000959:Antihypertensive Agents / Q000627:therapeutic use; D003928:Diabetic Nephropathies / Q000503:physiopathology; D005921:Glomerulonephritis / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology; D006977:Hypertension, Renal / Q000188:drug therapy* / Q000503:physiopathology; D007668:Kidney / Q000473:pathology; D007674:Kidney Diseases / Q000188:drug therapy / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000503:physiopathology; D009393:Nephritis / Q000503:physiopathology; D009400:Nephrosclerosis / Q000503:physiopathology; D051381:Rats; D011918:Rats, Inbred SHR; D014563:Urodynamics
D000959:Antihypertensive Agents