Effects of antihypertensive drugs on vascular remodeling: do they predict outcome in response to anti hypertensive therapy?

Remodeling of large and small arteries in hypertension contributes to eleva tion of blood pressure, and may participate in the complications of hyperte nsion. Large arteries exhibit increased lumen size, thickened media with in creased collagen deposition, and decreased compliance, which contributes to raised systolic blood pressure and pulse pressure. In small (resistance) a rteries smooth muscle cells are restructured around a smaller lumen, withou t true hypertrophy, particularly in milder forms of hypertension, whereas i n severe forms and in secondary hypertension hypertrophic remodeling has be en reported. Endothelial dysfunction occurs in many patients, with prevalen ce similar to that of left ventricular hypertrophy. Treatment with angioten sin-converting enzyme inhibitors, angiotensin receptor subtype I antagonist s and long-acting calcium channel blockers has corrected changes in large a nd small arteries in hypertensive patients. Treatment with fl-blockers did not modify either structure or function of small arteries. Improved outcome s were reported in clinical trials with drugs that exert vascular protectiv e effects, such as angiotensin-converting enzyme inhibitors and angiotensin receptor subtype 1 antagonists, as well as with those that do not appear t o improve vascular structure or function. Recent trials suggest that these different drugs may provide similar benefits essentially through blood pres sure lowering, although some minor differences between drugs have been note d. For example, the alpha -blocker doxasozin has been associated with worse outcomes (heart failure) than have diuretics. That hard end-point clinical trials have not demonstrated any advantages of agents with vasculoprotecti ve properties may relate in part to the relatively short duration of some o f these multicenter trials (3-5 years). Another contributing factor may be the low number of events with each drug class in the longer trials. Thus, c urrent evidence does not support the rational expectation that vasculoprote ctive antihypertensive agents will be associated with better outcomes in hy pertensive patients, possibly because of limitations of these trials. Curr Opin Nelphrol Hypertens 10:617-624. (C) 2001 Lippincott Williams & Wilkins.