Arterial protection: a neglected but crucial therapeutic goal. Hypertension is accompanied by 2 major types of arterial pathologic conditions: smooth muscle hypertrophy of arteriolar resistance vessels and atherosclerosis, primarily involving the larger arteries. Smooth muscle hypertrophy may develop either as a secondary defense against elevated intravascular pressure or as a primary defect responsible for the increased pressure. Insulin and a number of other trophic stimuli may play a pathogenetic role in vascular hypertrophy. Reducing blood pressure and trophic stimuli may cause hypertrophy to be reversed. Because atherosclerosis may be markedly accelerated by hypertension, especially in the presence of concomitant risk factors, such as hypercholesterolemia, cigarette smoking and diabetes mellitus, antihypertensive treatment may attenuate or even reverse the extent of atherosclerosis, but only when the causative factors are also corrected. Some commonly used antihypertensive agents, e.g., diuretics and beta blockers without intrinsic sympathomimetic activity, often aggravate hypercholesterolemia and glucose intolerance, thereby diminishing their potential protective value. Other types of drug therapy, such as alpha blockers, beta blockers with intrinsic sympathomimetic activity or other vasodilator activity, angiotensin-converting enzyme inhibitors and calcium entry blockers that may not induce biochemical changes, should provide better control of multiple risks and thereby better protection against atherosclerosis. With a better understanding of how hypertension induces arterial damage, clinicians will be able to provide more appropriate treatment and, it is hoped, alleviate such damage. 