When rats are treated with furosemide, there is a rapid natriuresis. However, increased sodium appetite does not occur until some time later. One hypothesis to explain this delay is that increased circulating levels of the hormones of sodium depletion prime or sensitize the brain circuits involved in sodium appetite, perhaps by induction of target gene(s). In the present study, we describe the time course of the temporal maturation of sodium appetite after furosemide treatment and the associated changes in plasma levels of ANG II and aldosterone and in plasma volume. Sodium appetite is modest 3 h after furosemide treatment, is increased after 12 h, and is still larger after 24 h. This pattern is evident with repeated testing. Plasma levels of aldosterone and plasma renin activity are substantially increased 3 h after furosemide treatment, and so the NaCl appetite cannot result simply from progressively increasing levels of these hormones. Furthermore, activation of the subfornical organ and the ventral lamina terminalis, assessed with c-Fos immunocytochemistry, did not differ across these three times. Metyrapone, an inhibitor of adrenal steroid synthesis, was used to examine sodium appetite in the absence of elevations in aldosterone after furosemide treatment. Although metyrapone effectively blocked the increase in aldosterone, it was without effect on the appetite 3 or 24 h after furosemide treatment. Furthermore, elevations of plasma aldosterone by the use of minipumps for several days before furosemide treatment did not prime or potentiate but instead tended to inhibit the induced sodium appetite, despite achieving levels of aldosterone and plasma renin activity typically associated with a robust sodium appetite. Infusions of DOCA gave a similar result. Lastly, minipump infusions of ANG II also did not potentiate sodium appetite. Thus neither addition nor subtraction of these hormones alone influenced sodium appetite under these conditions.

circumventricular organs; c-Fos; metyrapone; deoxycorticosterone acetate

This article has been cited by other articles:

				J. C. Geerling and A. D. Loewy Central regulation of sodium appetite Exp Physiol, February 1, 2008; 93(2): 177 - 209. [Abstract] [Full Text] [PDF]

				R. L. Thunhorst, T. G. Beltz, and A. K. Johnson Glucocorticoids increase salt appetite by promoting water and sodium excretion Am J Physiol Regulatory Integrative Comp Physiol, September 1, 2007; 293(3): R1444 - R1451. [Abstract] [Full Text] [PDF]

				J. C. Geerling and A. D. Loewy Sodium depletion activates the aldosterone-sensitive neurons in the NTS independently of thirst Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1338 - R1348. [Abstract] [Full Text] [PDF]

				Y. K. Cho, M. E. Smith, and R. Norgren Low-dose furosemide modulates taste responses in the nucleus of the solitary tract of the rat Am J Physiol Regulatory Integrative Comp Physiol, October 1, 2004; 287(4): R706 - R714. [Abstract] [Full Text] [PDF]

				N. E. Rowland, B. E. Goldstein, and K. L. Robertson Role of angiotensin in body fluid homeostasis of mice: fluid intake, plasma hormones, and brain Fos Am J Physiol Regulatory Integrative Comp Physiol, June 1, 2003; 284(6): R1586 - R1594. [Abstract] [Full Text] [PDF]