No abstract

The antihypertensive effect of eplerenone was equal in black and white patients and was superior to losartan in black patients.

The purpose of this study was to determine whether exercise training alters the sensitivity and responsiveness to insulin of glucose uptake and oxidation in fat cells. Female rats were exercised by swimming 6 h/day, 5 days/wk for 12 wk. The swimmers' fat cells were smaller than those of sedentary controls of the same age and similar body weight. A larger amount of insulin was specifically bound by fat cells of the trained rats because of an increase in the number of insulin receptors. The rates of 2-deoxyglucose uptake and of glucose oxidation were higher in fat cells of trained compared with sedentary rats at all insulin concentrations. A maximal insulin stimulus resulted in rates of sugar uptake and oxidation that were about sixfold higher in trained than in sedentary rats' fat cells. This greater responsiveness to insulin could not be explained by the increase in insulin binding but appears to be mediated by adaptation/s) at a step(s) beyond the binding of insulin to its receptors. Our findings suggest that fat cells of exercise-trained animals are adapted for rapid replenishment of energy stores.

Muscle contractile activity results in an increase in glucose uptake rate that can persist for hours. This study was undertaken to determine the effect of carbohydrate repletion on reversal of an exercise-induced increase in glucose uptake. Rats were exercised by swimming. In rats studied 60 min after exercise, muscle glycogen content was 75% depleted and glucose uptake rate was increased. The effect of exercise on glucose uptake was reversed, and glycogen concentration had increased 44 mumol/g muscle, within 18 h in rats fed carbohydrate. In rats fed a carbohydrate-free diet, muscle glycogen increased only 11 mumol/g, and glucose uptake rate had returned only 50% of the way to base line 18 h after exercise. The rate of 3-methylglucose accumulation in muscles was increased sixfold 60 min after exercise. This increase in permeability to sugar was reversed within 18 h in rats fed carbohydrate. In rats fed a carbohydrate-free diet the rate of 3-methylglucose accumulation was still threefold above base line 18 h after exercise. Our results provide evidence that decreased availability of carbohydrate slows reversal of an exercise-induced increase in permeability of muscle to sugar.

U ntil recently, the importance of aldosterone in the development of hypertension has been underestimated and the assumption made that aldosterone-mediated effects could be adequately controlled with angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs). However, long-term ACE inhibitor or ARB therapy may not adequately protect patients from the effects of aldosterone escape [1][2][3] -an effect that can be minimized by blocking aldosterone at the mineralocorticoid receptor. 4A growing body of clinical evidence has linked aldosterone to the development of hypertension, cardiac hypertrophy, cardiac and vascular fibrosis,