Aspects of the role of intraglomerular pressure as a cause of progressive renal damage.

Renal damage in hypertension was thought to be a result of excessive renal arteriolar constriction leading to ischaemia and nephron damage. However, more recent studies have shown that in animal models the aetiology is one of increased intraglomerular pressure, and there is strong evidence that this is also the case in patients with essential hypertension. The problem is therefore one of inadequate constriction of afferent arterioles allowing increased systemic pressure to be transmitted to the glomerular capillaries. Since angiotensin II preferentially constricts the efferent arterioles, and since hypertensive patients have increased renovascular sensitivity to angiotensin II, this may explain why angiotensin-converting enzyme inhibitors are the only drugs which actually lower intraglomerular pressure and why they reduce renal damage in hypertensive disease.