Abstract
The effects of selective destruction of the catecholamine innervation of the nucleus tractus solitarii (NTS) on arterial pressure (MAP) and heart rate (HR) were examined in unanesthetized rats in which 6-hydroxydopamine (6-OHDA), 1 .mu.l, was injected bilaterally into the nucleus at the level of the obex. Control rats received 1 .mu.l of vehicle or were uninjected. Baroreceptor reflex activity was tested by measuring the reflex bradycardia in response to graded doses of phenylephrine. A 2 .mu.g dose of 6-OHDA, did not alter MAP or HR; 12 .mu.g, a dose producing necrosis of NTS, resulted in the development within 4-6 h of fulminating arterial hypertension and tachycardia. A 4 .mu.g dose of 6-OHDA produced an elevation of MAP which returned to control levels by 48 h without changing HR. By 6 h, the arterial pressure became extremely labile. Lability of MAP in the absence of hypertension or change of HR persisted for the longest period of observation, 2 wk. Baroreceptor reflex activity remained, although the sensitivity of thr reflex was depressed. The 4 .mu.g dose of 6-OHDA failed to produce histological damage to NTS. Biochemically, it resulted after 14 days in a reduction of the activity of dopamine .beta.-hydroxylase, a specific marker of noradrenergic and adrenergic neurons, to 40% of control without altering the activity of choline acetyltransferase, a marker of cholinergic neurons. Selective removal of a substantial portion of the catecholamine innervation of the NTS, mostly noradrenergic, results in persistent lability without elevation of arterial pressure. The catecholamine innervation of NTS modulates rather than mediates baroreceptor reflexes, serving to maintain arterial pressure within narrow limits.