ACUTE SALINE INFUSION DECREASES NOREPINEPHRINE RELEASE IN THE ANTERIOR HYPOTHALAMIC AREA

Ingestion of a high NaCl diet elevates arterial pressure in spontaneou sly hypertensive rats, at least in part, by reducing the release of no repinephrine in the anterior hypothalamic area. The mechanism by which dietary NaCl excess alters anterior hypothalamic area norepinephrine release is unknown. Plasma Na+ is slightly elevated after ingestion of a meal; therefore, in the present study we tested the hypothesis that a small increase in plasma Na+ could reduce the release of norepineph rine in the anterior hypothalamic area and elevate arterial pressure. Male spontaneously hypertensive rats were randomized to be fed a diet containing either 1% (basal) or 8% (high) NaCl at age 7 weeks and were maintained on the diets for 2 weeks. Age-matched normotensive Wistar- Kyoto rats received a basal NaCl diet only. All rats were instrumented with a push/pull cannula, and 5 days later, the baseline release of 3 -methoxy-4-hydroxyphenyl glycol (the major metabolite of norepinephrin e in brain) was measured in awake, freely moving rats. Rats were then challenged with an intravenous infusion (75 mu L/min) of hypertonic (2 .7%) saline for 20 minutes. In spontaneously hypertensive rats fed a b asal NaCl diet, the hypertonic saline infusion elevated mean arterial pressure by 12% and reduced the concentration of the norepinephrine me tabolite in the anterior hypothalamic area by 19%; these alterations p ersisted after termination of the hypertonic saline infusion. Spontane ously hypertensive rats maintained on the high NaCl diet showed greatl y reduced arterial pressure and norepinephrine metabolite responses. I n normotensive control rats compared with the hypertensive rats fed th e basal NaCl diet, the hypertonic saline had considerably less effects on arterial pressure and norepinephrine metabolite levels in the ante rior hypothalamic area, and the responses were significantly shorter. Thus, a small elevation in plasma Na+ can reduce the release of norepi nephrine in the anterior hypothalamic area. This response is greatly e xaggerated in spontaneously hypertensive rats fed a basal (but not a h igh) NaCl diet, suggesting that a postprandial rise in NaCl could init iate the fall in norepinephrine and thereby contribute to the rise in arterial pressure in spontaneously hypertensive rats ingesting a high NaCl diet.