Regression of structural cardiovascular changes by antihypertensive therapy.
Structural vascular changes, consisting mainly of smooth muscle cell hypertrophy of the arterioles, have been found in various hypertensive animal models as well as in hypertensive patients. Although such changes may be to some extent a primary phenomenon in primary or essential hypertension, there is ample proof that an elevation in arterial pressure over a period of time will cause hyperplasia of the media in the resistance vessels; thus, this change is secondary to the rise in pressure. Studies in various animal models have shown that such structural arteriolar changes are reversible if a long-term reduction in arterial pressure can be obtained. In hypertensive patients reversibility of such changes has been demonstrated in some vascular beds as a result of chronic antihypertensive therapy. However, no complete "normalization" has ever been shown, probably because of inadequate reduction of arterial pressure and perhaps also because long-standing hypertension induces fibrosis of the arteriolar media, which is less likely to be positively affected by a lowering of blood pressure. In humans, some vascular beds, for example, the muscle vessel bed of the calves, appear to be less suitable for the demonstration of regression of structural changes. This could be due to erect posture, which increases the transmural pressure in these vessels, since the effect of gravity is added to the intravascular pressure. Finally, it is conceivable that effects other than the reduction in arterial pressure could play a role. Thus, antihypertensive drugs with a vasodilating action appear to be more effective in reducing structural vascular changes than drugs that do not have a vasodilating effect, even if an identical degree of blood pressure reduction is obtained.(ABSTRACT TRUNCATED AT 250 WORDS)
D001132:Arm / Q000098:blood supply; D001158:Arteries / Q000473:pathology*; D001160:Arterioles / Q000473:pathology*; D006801:Humans; D006973:Hypertension / Q000473:pathology*; D009132:Muscles / Q000098:blood supply; D010991:Plethysmography; D012867:Skin / Q000098:blood supply