Clinical and experimental diabetic states are often characterized by an increase in the glomerular filtration rate, and early hyperfiltration may be a risk factor for the later development of diabetic glomerulopathy. Evidence in diabetic animal models suggests that, of the determinants of diabetic hyperfiltration, glomerular capillary hypertension plays a key role in the development of structural injury. In diabetic rats, despite normal systemic blood pressure, the glomerular capillary pressure is elevated because of disproportionate vasodilation of the afferent arteriole. In this normotensive model, a modest reduction in systemic blood pressure with angiotensin I-converting enzyme inhibitor therapy normalizes glomerular capillary pressure and retards the development of injury. However, animal studies suggest that all antihypertensive regimens may not afford equivalent protection. It has been reported that monotherapy with calcium channel blockers, or hydralazine, is less effective in limiting albuminuria than are angiotensin-converting enzyme inhibitors. In a study comparing the effects of angiotensin-converting enzyme inhibitors with those of reserpine, hydrochlorothiazide, and hydralazine, both regimens lowered blood pressure and offered some long-term protection. However, angiotensin-converting enzyme inhibition resulted in significantly greater limitation of injury than did the combination regimen. These results suggest that antihypertensive therapy retards diabetic renal disease; however, some antihypertensive regimens may afford superior protection.
|Original language||English (US)|
|Journal||Journal of the American Society of Nephrology|
|Issue number||5 SUPPL.|
|Publication status||Published - Nov 1990|
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