Fourteen maintenance hemodialysis patients volunteered to participate in a 6-month program of exercise training. The exercise was performed on a stationary bicycle during the hemodialysis treatment. Six maintenance hemodialysis patients served as control without exercise training. Exercising patients participated in 91% of all possible exercise sessions. The exercise group showed a significant (23%) increase in maximal oxygen consumption over the 6 months. No change in exercise capacity resulted in the control group. Five of eight hypertensive patients in the exercise group decreased or discontinued antihypertensive medications. No changes occurred in hematocrit or lipid profiles in either group. We conclude that exercise training during the hemodialysis treatment is technically feasible and safe for appropriately screened patients and will increase exercise capacity, and in some patients improve blood pressure control. Exercise during dialysis also improves compliance to regular exercise and facilitates supervised exercise sessions, which are desirable in this patient group.

A B S T R A C T In order to determine whether or not antidiuretic hormone (ADH) is essential to the inhibition of an acute water diuresis in adrenal insufficiency, the response to oral water loads was tested in rats with hereditary hypothalamic diabetes insipidus (DI) which lack ADH. It was found that 60 min after water loads of 3 or 5% of body weight urine flow was significantly lower and urine osmolality significantly higher in adrenalectomized DI rats than in the same DI rats before removal of their adrenal glands.The efficacy of gluco-and mineralocorticoids in reversing the inhibition was then determined in the same adrenalectomized DI rats. Prednisolone alone, administered either acutely or chronically, restored the response in urine flow to that seen in the same rats before adrenalectomy, but failed to correct the defect in urinary dilution. Aldosterone when given alone tended to correct the diluting ability but not the response in urine flow. When these two adrenal cortical hormones were given simultaneously, both the urine flow and urine osmolality were nearly identical to what they had been in the same DI rats before adrenalectomy. These studies strongly suggest (a) that ADH is not essential to the inhibition of an acute water diuresis in adrenal insufficiency, although it may abet the inhibition in individuals without diabetes insipidus, which can elaborate ADH; and (b) that both gluco-and mineralocorticoids are required in adrenal insufficiency in order to fully restore the water diuresis as judged by the dual criteria of urine flow and urine osmolality. INTRODUCTIONThe mechanism by which an acute water diuresis is inhibited in adrenal insufficiency has been the subject of intensive investigation and debate. (For a list of references, see reference 1.) Although changes such as decreased extracellular fluid volume or decreased glomerular filtration rate (GFR) may contribute to the inhibition, it seems clear that these are not the only, or even the major, factors involved. The main current controversy centers about the role of the antidiuretic hormone (vasopressin or ADH). One view states that in adrenal insufficiency water diuresis is inhibited by sustained high blood concentrations of ADH because in the absence of adrenal corticoids, secretion of ADH from the posterior pituitary gland cannot be shut off (2). Proponents of the second view contend that ADH has little to do with the inhibited water diuresis, but rather, that the adrenal steroids alter the water permeability of the distal renal tubules and collecting ducts (3). Both views have been supported by results of bioassays, the first showing sustained, high concentration of ADH in the blood of patients with adrenal insufficiency even after an acute water load (2), the second showing undetectable blood levels of ADH under similar circumstances (3).

A B S T R A C T This study utilized rates with hereditary hypothalamic diabetes insipidus (D.I.) in order to explore possible mechanisms which prevent full urinary concentration after acute administration of vasopressin in hypothalamic D.I. and which correct this concentrating defect with prolonged therapy.It was found: (a) that the concentrating defect persisted even when the urinary osmolal excretion of D. I. rats was reduced to that of normal animals; (b) that the defect was not corrected more rapidly if larger doses of vasopressin were given; (c) that it persisted even when the D.I. rats were deprived of drinking water after vasopressin was given; (d) that there was osmotic equilibration between urine and renal papilla at a time when the concentrating defect was still evident; and (e) that the correction of the defect was associated with progressive and significant rise of the papillary osmolality.These studies appear to rule out osmotic diuresis, accumulation of exogenous vasopressin, persistent primary polydipsia, or delay in the induction of membrane permeability as causes for the concentrating defect. Rather, subnormal osmolality of the renal papilla, which can be corrected only gradually, accounts for the initial concentrating Dr. Harrington's present address is

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