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Sodium balance and aldosterone during dehydration and rehydration in the dog
Ist Teil von
American journal of physiology. Regulatory, integrative and comparative physiology, 1984-07, Vol.247 (1), p.76-R83
Ort / Verlag
Bethesda, MD: American Physiological Society
Erscheinungsjahr
1984
Quelle
MEDLINE
Beschreibungen/Notizen
T. N. Thrasher, C. E. Wade, L. C. Keil and D. J. Ramsay
The regulation of sodium metabolism and the renin-angiotensin-aldosterone
system was evaluated during 24 h of water, but not food, deprivation and
during rehydration in the dog. Dehydration caused increases in plasma
concentrations of sodium (6.0 +/- 0.7 meq/l), protein (0.8 +/- 0.1 g/dl),
vasopressin (5.3 +/- 0.9 pg/ml), and renin activity (3.5 +/- 1.1 ng AI X
ml-1 X 3 h-1). Plasma aldosterone was unchanged and plasma potassium fell
slightly (0.2 +/- 0.1 meq/l). During dehydration, food, and thus sodium
intake fell by more than 10% in 12 of 19 dogs, but urinary sodium excretion
increased significantly, leading to a negative sodium balance (1.9 +/- 0.2
meq/kg). Sodium retention was observed after rehydration and sodium
balance; plasma electrolytes, vasopressin, and plasma renin activity (PRA)
returned turned to control levels after the 1st day of recovery. However,
plasma aldosterone was slightly elevated at this time, returning to control
after the 2nd day of recovery. The dehydration-induced natriuresis could
not be accounted for by a fall in plasma aldosterone. However, sodium
retention following rehydration could be aldosterone dependent, because
additional studies showed a threefold rise in plasma levels of the hormone
1 h after drinking. The acute rise in aldosterone correlated closely (r =
0.82) with the fall in plasma sodium after drinking but not with changes in
adrenocorticotrophic hormone, PRA, or plasma potassium. It is concluded
that natriuresis is a homeostatic response to dehydration as a means of
ameliorating the rise in body fluid osmolality.