AJP - Regulatory, Integrative and Comparative Physiology, Vol 244, Issue 6 810-R814, Copyright © 1983 by American Physiological Society
Lowered cerebrospinal fluid sodium antagonizes effect of raised blood sodium on salt appetite
A. F. Muller, D. A. Denton, M. J. McKinley, E. Tarjan and R. S. Weisinger
Moderately Na-deficient sheep (i.e., Na deficit = 300-400 mmol) will
correct their deficit when given hypertonic NaHCO3 solution to drink.
Access to NaHCO3 was provided by bar press for 2 h only each day following
22 h of salivary loss from a parotid fistula. Each delivery by bar press
provided 9 mmol of NaHCO3 and, of the 46.3 +/- 2.5 deliveries made and
drunk in 2 h, 80-90% were made in the first 20 min. Ten minutes before
access to NaHCO3 commenced an intracarotid infusion of 4 M NaCl at 1.6
ml/min for 30 min was initiated. This infusion reduced intake by
approximately 80% and increased both plasma and cerebrospinal fluid sodium
concentration (CSF[Na]). Intraventricular (ivt) infusion of 0.7 M mannitol
in artificial CSF at 1 ml/h for 3 h begun 1 h before access to Na by bar
press lowered CSF[Na] and approximately doubled voluntary Na intake. The
combination of the two procedures resulted in NaHCO3 intake similar to base
line. That is, the ivt infusion of 0.7 M mannitol counteracted the
inhibition of Na appetite produced by the systemic infusion of hypertonic
NaCl, and this was associated with attenuation of the effect of the
systemic 4 M NaCl infusion on CSF[Na]. The results suggest that the effects
of both the ivt and the systemic infusions are mediated via the same sensor
system located within the neuropil.
