Effects of calcium channel blockers on experimental glomerular injury.
A major problem for patients with kidney disease is that most chronic renal diseases progress to endstage renal failure. Studies in experimental models of hypertension and renal insufficiency suggest that progressive glomerular sclerosis may be the long-term consequence of functional and structural adaptations of the kidney to a moderate loss of filtration capacity. In a number of settings, sclerosis has been related to the presence of an elevated glomerular capillary hydraulic pressure. A growing body of evidence also supports the hypothesis that kidney hypertrophy and glomerular hypertrophy constitute independent risk factors for glomerular sclerosis. Recent studies suggest that calcium antagonists can reduce glomerular injury in experimental hypertension. Renal protection may be related to the ability of these agents to reduce glomerular pressure and/or inhibit compensatory renal growth.
Dworkin
L D
LD
Department of Medicine, New York University Medical Center, 550 Fust Avenue, New York, NY 10016, USA.
D000818:Animals; D002118:Calcium / Q000037:antagonists & inhibitors; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D003900:Desoxycorticosterone / Q000494:pharmacology; D004195:Disease Models, Animal; D005923:Glomerulosclerosis, Focal Segmental / Q000188:drug therapy* / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000628:therapy; D007668:Kidney / Q000254:growth & development; D007676:Kidney Failure, Chronic / Q000188:drug therapy*; D007678:Kidney Glomerulus / Q000293:injuries*; D011312:Pressure; D051381:Rats; D011918:Rats, Inbred SHR
D002121:Calcium Channel Blockers; D003900:Desoxycorticosterone; D002118:Calcium