Ne. Rowland et al., AGING AND FLUID HOMEOSTASIS IN RATS, American journal of physiology. Regulatory, integrative and comparative physiology, 42(4), 1997, pp. 1441-1450
The capacity of aging rats to defend body fluid homeostasis in respons
e to a variety of dipsogenic and natriorexigenic stimuli was assessed.
Male and female rats of both the Fischer 344 (FR) and Sprague-Dawley
(SD) strains were used and tested at target ages of similar to 5, 10,
15, and 20 mo in both longitudinal and cross-sectional studies. There
were no consistent age-related declines in water intake in response to
water deprivation or acute administration of hypertonic NaCl; angiote
nsin (ANG) I, II, III; or isoproterenol. Likewise, there were no major
impairments in either urinary excretion of the hypertonic NaCl load o
r excretion of water or hypotonic NaCl loads, although the latter were
excreted more slowly in the older cohorts. The preference/aversion fu
nctions for NaCl solutions differed between SD and FR rats, but did no
t change with age except in male FR rats that lost their aversion to d
ilute NaCl at 20 mo of age. Intake of hypotonic NaCl solution after ac
ute sodium depletion (furosemide treatment) showed a partial decline w
ith age, and the older rats sustained larger estimated sodium deficits
after a 6-h repletion period. A more complete age-related decline was
observed in the intake of hypertonic NaCl stimulated by chronic dieta
ry administration of a kininase II inhibitor (ramipril). Male rats of
15-20 mo of age showed no ramipril-induced sodium appetite. Brain ANG
II receptor density, determined by autoradiography, declined by almost
50% in the paraventricular nucleus at 20 mo of age and declined sligh
tly in the organum vasculosum laminae terminalis but did not decline i
n either the supraoptic nucleus or subfornical organ. Thus the major d
eficits in fluid intake in aging rats are related to salt appetite; th
e mechanism was not identified definitively.