AJP - Regulatory, Integrative and Comparative Physiology, Vol 248, Issue 4 464-R470, Copyright © 1985 by American Physiological Society
Disordered drinking in developing spontaneously hypertensive rats
F. S. Kraly, L. A. Coogan, S. M. Specht, M. S. Trattner, C. Zayfert, A. Cohen and J. A. Goldstein
Eating and drinking in spontaneously hypertensive (SHR) and Wistar-Kyoto
(WKY) rats were measured at 5-17 wk of life. The SHR drank significantly
more water in 24 h than WKY as early as wk 9, spilled more dry food than
did WKY, and exhibited an inverse relation between 24-h water intake and
dry food spilled. When eating a meal of dry food after 12 h food
deprivation, SHR drank earlier and drank more in a 1-h test than WKY rats.
Moreover, SHR exhibited (as early as wk 7) a striking pattern of
interrupting eating to drink. This pattern was not present when SHR ate
liquid food, and it was attenuated by infusion of water through a cheek
fistula. Adult SHR (22 wk) salivated less than WKY in response to
intraperitoneal 3.25 mg/kg pilocarpine nitrate. When developing SHR and WKY
were maintained on liquid and solid food, SHR gained disproportionately
more weight than WKY during development. When young SHR were permitted to
drink no more water than WKY rats, the development of hypertension was
retarded, and body weight gain was slowed. Because restricted access to
food, which produced an equivalent slowing of body weight gain as did
restricted access to water, also retarded development of hypertension, it
appears that restricted access to water retards development of hypertension
due to delayed growth. These results demonstrate that hyperdipsia,
apparently caused by deficient salivary function, is not necessary for the
development of hypertension in SHR.
