ACUTE HYPERTENSION INCREASES NOREPINEPHRINE RELEASE IN THE ANTERIOR HYPOTHALAMIC AREA

Neurons in the anterior hypothalamic area play an important role in Na Cl-sensitive hypertension in spontaneously hypertensive rats, and prev ious studies have suggested that baroreceptor feedback modifies the ac tivity of these neurons. To test the hypothesis that the release of no repinephrine in the anterior hypothalamic area is modified by arterial baroreceptor reflex feedback and that this reflex release is disturbe d in spontaneously hypertensive rats on a high NaCl diet, we used the push-pull technique to measure the release of the norepinephrine metab olite 3-methoxy-4-hydroxy-phenylglycol in the anterior hypothalamic ar ea. Seven-week-old male spontaneously hypertensive and normotensive Wi star-Kyoto rats were placed on a high (8%) or a basal (1%) NaCl diet f or 2 weeks. The high NaCl diet elevated mean arterial pressure and gre atly reduced basal norepinephrine metabolite levels in the anterior hy pothalamic area of the spontaneously hypertensive (but not the control ) rats (305+/-32 pg/10 min in the rats consuming 1% NaCl and 93+/-9 pg /10 min in the rats consuming 8% NaCl). An infusion of tramazoline (an imidizoline that causes long-lasting hypertension) that increased art erial pressure by 25 mm Hg elevated anterior hypothalamic area norepin ephrine metabolite concentrations significantly more in the spontaneou sly hypertensive rats on the 1% NaCl diet (to 392+/-46 pg/10 min) than in those on the 8% NaCl diet (to 113+/-18 pg/10 min). In contrast, in Wistar-Kyoto rats the tramazoline-induced increase in arterial pressu re elevated anterior hypothalamic area norepinephrine metabolite conce ntrations slightly more in rats on the 8% NaCl diet than in those on t he 1% NaCl diet. These data suggest that baroreflex activation increas es norepinephrine release in the anterior hypothalamic area of the awa ke rat and that a high NaCl diet blunts this response in spontaneously hypertensive (but not Wistar-Kyoto) rats.