Perfusion of the isolated, rat hind limb was performed during conditions of rest and exercise. The rate of blood tlow increased progressively from onset of perfusion in both the control and stimulated preparations with no significant difference between the two groups, whereas glucose disappearance from the perfusate was greatly accelerated during exercise. Tbe exercised limb extracted more glucose from the blood than the control preparation, in spite of a lower glucose concentration and a diminished volume of perfusate passing through the musc1e during the same period of time. Glucose uptake remained elevated during the entire period of electrical stimulation of the motor nerves, even though the amplitude of musc1e movements gradually dirninished with time.

Diabetes mellitus and hypertension constitute two powerful independent risk factors for cardiovascular, renal and atherosclerotic disease. The frequent occurrence of the two diseases in the same individual doubles the risk of cardiovascular death, as well as substantially increasing the frequency of transient ischemic attacks, strokes, peripheral vascular disease with lower extremity amputations, as well as end-stage renal disease and blindness. Although hypertension usually occurs in IDDM in association with renal disease, in NIDDM the evolution of hypertension appears to be multifactorial and independent of renal disease. Obesity appears to be dissociable from hypertension and NIDDM with a common link between obesity, hypertension and NIDDM appearing to be hyperinsulinism and insulin resistance. It has been suggested that hyperinsulinism and insulin resistance may lead to hypertension through altered intracellular calcium metabolism, enhanced renal sodium reabsorption, or through an effect of insulin upon lipid and/or catecholamine metabolism. Further, insulin itself may have a direct effect upon the atherosclerotic process in the hypertensive diabetic patient. These considerations have been taken into account in the structuring of antihypertensive therapy in Type I and Type II Diabetes Mellitus.

In lIitro basal and insulin stimulated glucose metabolism (14 C02 production and 14 C glucose incorporation into fatty acids) are enhanced in the epididymal fat pads of fed Sprague Dawley rats exposed to intraperitoneal growth hormone (GA) both acutely (90 minutes after a single 1 mg injection) and chronicaUy (24 hours after the last of a 15 day series of 1 mg GA injections). This enhancement of the glucose metabolism in the fat pad is accompanied by depletion of its lipid conten!. This alteration in glucose metabolism in adipose tissue exposed to GH ;n 11;110 may be related to the action of GH in accelerating intracellular free fally aeid turnover and/or may be subsequent to a decrease in the size of the fat cello

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