Key result
NTS catecholamine destruction in rats causes persistent arterial pressure lability without altering heart rate.
Why the study?
The role of the catecholamine innervation of the nucleus tractus solitarii in modulating arterial pressure and baroreceptor reflexes was unclear.
Does selective destruction of catecholamine innervation of the NTS alter arterial pressure and heart rate in rats?
Does selective destruction of catecholamine innervation of the NTS alter arterial pressure and heart rate in rats?
Selective removal of catecholamine innervation of the NTS in rats results in persistent lability of arterial pressure without chronic elevation, suggesting these neurons modulate rather than mediate baroreceptor reflexes.
Selective NTS catecholamine depletion produces chronic BP lability in rats; leaves open its role in human baroreflex modulation.
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 ;J, was injected bilaterally into the nucleus at the level of the obex.Control rats received 1 fil of vehicle or were uninjected.Baroreceptor reflex activity was tested by measuring the reflex bradycardia in response to graded doses of phenylephrine.6-OHDA, 2 /ig, did not alter MAP or HR; 12 /ig, a dose producing necrosis of NTS, resulted in the development within 4-6 hours of fulminating arterial hypertension and tachycardia.6-OHDA, 4 fig, produced an elevation of MAP which returned to control levels by 48 hours without changing HR.By 6 hours, however, 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 weeks.Baroreceptor reflex activity remained, although the sensitivity of the reflex was depressed.6-OHDA, 4 /ig, failed to produce histological damage to NTS.Biochemically, it resulted after 14 days in a reduction of the activity of dopamine /3-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.We conclude that 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 results suggest that the catecholamine innervation of NTS modulates rather than mediates baroreceptor reflexes, serving to maintain arterial pressure within narrow limits.THE NUCLEUS tractus solitarii (NTS), a nucleus of the medulla oblongata, plays an essential role in the central neural integration of cardiovascular activity.The intermediate region of the nucleus, located at the level of the obex, serves as the primary relay area for arterial baro-and chemoreceptor reflexes.1 " 3 Bilateral lesions of this area result not only in the abolition of arterial baroreceptor reflexes, 4 " 6 but also in the development of neurogenic arterial hypertension, fulminating in rats 4 ' 5 ' 7 and chronic and labile in cats.6 The NTS and adjacent regions of the dorsal medulla are richly innervated by catecholaminecontaining neurons.8 " 11 It has been presumed on the basis of histofluorescence that most of the catecholamine-containing fibers innervating NTS are From the
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Snyder et al. (1978) studied this question. 6-hydroxydopamine (6-OHDA) vs. Vehicle or uninjected was evaluated on Arterial pressure (MAP) and heart rate (HR). Selective destruction of catecholamine innervation of the NTS with 4 µg of 6-OHDA in rats resulted in persistent lability of arterial pressure without elevation of arterial pressure or change in HR.
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