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Response and regulation of vasopressin and renal function during graded exercise
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|Title:||Response and regulation of vasopressin and renal function during graded exercise|
|Authors:||Wade, Charles E.|
Kidney function tests
Exercise -- Physiological aspects
|Abstract:||Three series of experiments were conducted to study the response and regulation of plasma vasopressin during exercise. The renal handling of water and solutes during exercise was also investigated. Six male subjects, performed a graded exercise test on a treadmill to voluntary maximal effort. Three additional experiments were performed; a control and 1 hr of exercise at 35 and 70% of maximum heart rate. Blood samples were obtained at 20 and 60 min of exercise and after 1 hr of recovery. Urine samples were also obtained. Plasma vasopressin (PAVP) was unchanged during controls and 35% exercise and elevated following 60 min of 70% exercise, from 0.8 ± 0.2 at rest to 2.1 ± 0.3 µU/ml. This elevation persisted through recovery. Maximal exercise produced an increase in PAVP from 0.9 ± 0.1 to 2.7 ± 0.7 µU/ml after 20 min. Plasma vasopressin returned to resting levels following 1 hr of recovery. Plasma osmolality, blood pressure, plasma renin activity (PRA), and oral temperature were elevated during exercise. Plasma volume and body weight decreased. Plasma cortisol exhibited no change. A reduction of vasopressin metabolism may have occurred, contributing to the elevation of PAVP. There was no consistent relationship of changes in these parameters to the elevation of PAVP during exercise. Urine flow was decreased for both 70% and maximal exercise post-exercise and after 1 hr of recovery. The decrease immediately after exercise was accompanied by a decrease in creatinine clearance and osmotic clearance (Cosm) and an increase in CH2O. Recovery Cosm was decreased, CH2O increased, and creatinine clearance normal. The response of vasopressin to an elevation in body temperature was studied in seven males. The subjects underwent a 2-hr equilibration period, a l-hr experimental exposure, and 2 hr of recovery. The experimental exposures were a control, exercise, and passive elevation of body temperature, in a manner similar to that observed during exercise. Five-hour urine samples were obtained. No difference was noted in rectal temperature during exercise and passive temperature elevation. Urine flow was significantly reduced during exercise compared to control values. Vasopressin excretion was increased 22,79, and 17% for control, exercise, and passive temperature elevation, respectively. The increase in the excretion of vasopressin with exercise occurred in six of the seven subjects with no change seen during passive body temperature elevation. Seven subjects performed maximal exercise following dehydration (10 hr of fasting) and hydration (ingestion of 300 ml of water). The pre-exercise plasma osmolaiity of 283 ± 2 mOsm/kg for hydration was lower than that of dehydration (288 ± 2 mOsm/kg). Following exercise no difference was observed in osmolality. Plasma vasopressin after exercise was elevated, 0.6 ± with hydration and 1.8 ± 0.6 µU/ml with dehydration. No differences in PRA, plasma cortisol, mean arterial pressure, oral temperature, change in plasma volume, or workload and duration were noted between the two treatments. Urine flow was greater during hydration pre-exercise and post-exercise compared to dehydration. Post-exercise urine flow was reduced with dehydration, and for both treatments flow was reduced during recovery. Osmotic clearance was reduced post-exercise and through recovery, while CH2O was increased post-exercise with dehydration. Plasma vasopressin was elevated during exercise and appeared to be dependent on the hydration state of the individual, work intensity, and duration. Although the regulation of vasopressin during exercise was unclear, the elevation of vasopressin appeared to be independent of the dehydration which occurred during exercise. The elevation of PAVP apparently was not responsible for the occurrence of the antidiuresis associated with exercise, which was probably due to a reduction in glomerular filtration rate and sodium reabsorption.|
Thesis (Ph. D.)--University of Hawaii at Manoa, 1979.
Bibliography: leaves 86-97.
xii, 97 leaves ill. 29 cm
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|Appears in Collections:||Ph.D. - Biomedical Sciences (Physiology)|
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