The pathophysiologic basis for blocking the renin-angiotensin system in hypertensive patients with renal disease.

The current understanding of the interrelationships among hemodynamic, hormonal, and metabolic factors in the pathophysiology of renal disease remains incomplete. In the kidney, the renin-angiotensin system (RAS) plays an important role in all three of these physiologic pathways. There is no doubt that hypertension and diabetes are major risk factors for the progression of renal disease and that interruption of the RAS is renoprotective. In particular, the balance of interactions between angiotensin II and nitric oxide is a key factor in determining whether injury or protection of target organs ensues. Experimental studies suggest a novel link between hemodynamic and metabolic factors that may cooperate to induce progressive glomerular injury in conditions characterized by glomerular hypertension. Emerging data from experimental and clinical studies may lead to improvements in therapeutic efforts to prevent or slow the progression of renal disease.