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Do ACE inhibitors protect the kidney from hemodynamically mediated glomerular injury in hypertensive renal disease?
Do ACE inhibitors protect the kidney from hemodynamically mediated glomerular injury in hypertensive renal disease?
This review highlights the pharmacological mechanisms by which ACE inhibitors may protect the kidney from hemodynamically mediated glomerular injury in hypertensive renal disease.
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Highlights mechanisms for ACE inhibitor renoprotection via hemodynamic control; leaves open validation in clinical trials.
Recent experimental studies suggest that the resistance state of the preglomerular and postglomerular capillary arterioles may determine if a particular class of antihypertensive agents will protect the kidney from hemodynamically mediated glomerular injury. This review discusses (1) the effects of angiotensin II on the renal microcirculation, (2) the pathophysiology of essential hypertensive renal disease, (3) the renal pharmacology of angiotensin-converting enzyme (ACE) inhibitors, and (4) the hypothesis that renal protection is dependent on control of systemic and glomerular hypertension.
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Bauer et al. (1991) studied this question.
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