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Hypertension and obesity are two disorders that have been closely related, each occurring in greater frequency with the other than in an otherwise normal population. Although a causal relationship has not been established between the two, their coincidence carries increased risk of cardiovascular morbidity and mortality. This report summarizes the pathophysiological studies from our laboratory concerning their interrelationship and offers a rational hypothesis for the mechanisms underlying this enhanced risk. Patients with hypertension demonstrate an increased total peripheral resistance that explains hemodynamically the rising arterial pressure with advancing vascular disease. In response to this increased afterload imposed upon the heart, the left ventricle adapts itself structurally through a process of concentric hypertrophy. In addition, in most patients with essential hypertension, plasma volume progressively contracts and renal vascular resistance increases in proportion to the rise in arterial pressure and total peripheral resistance. In contrast, in obesity-hypertension there is a superimposed factor of volume overload upon the hemodynamic abnormality. The result is an additional cardiac stimulus for eccentric hypertrophy due to the increased ventricular preload. This factor enhances left ventricular stroke work and its attendant myocardial oxygen demands, thereby providing a dual overload on cardiac function that can explain the increased risk of heart failure related to these associated conditions. In contrast to the compounding adverse hemodynamic effects on the heart, there does not seem to be an additive hemodynamic effect of obesity on hypertensive renal vascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)