Abstract
Hypertension is a systemic vascular disease that makes its mark upon the "target organs"--heart, brain, and kidneys--through the hemodynamic hallmark of the disease, a progressively increasing vascular resistance to the forward flow of blood. The effect of pressure overload upon the heart is one of concentric hypertrophy of the left ventricle that is, in turn, associated with an independent risk of morbidity and mortality. Reduction of arterial pressure reverses the risk associated with the elevated arterial pressure and also diminishes the risk from hemorrhagic and thrombotic strokes. Why the risk of the interaction of hypertensive and atherosclerotic diseases can be reduced on the brain but not as impressively on the heart remains to be learned, but certain recent lines of clinical and experimental evidence point to some answers. The issue as to why, in the face of increasing numbers of patients receiving the benefits of therapy, there is an alarming increase in patients with end-stage renal disease defies more imagination and study. Thus, many of the old questions seem to be achieving some meaningful answers; but associated with these new answers we are confronted with new questions.
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