Pressor responsiveness of the sub-retrofacial nucleus and the midbrain reticular formation in the rat after 6-hydroxydopamineinduced lesions of ascending and descending catecholamine pathways

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We have recently shown that intracerebroventricular (icvt) administration of 6-hydroxydopamine (6-OHDA) inhibits centrally-evoked pressor activity [1]. To see whether this effect is attributable to the disruption of descending bulbospinal or, alternatively, ascending suprabulbar catecholamine (CA) pathways, spontaneously hypertensive rats (SHR) were given localized intracerebral injections of 6-OHDA. One month later, pressor responses evoked by electrical or chemical stimulation in the rostral ventrolateral medulla or midbrain were examined under urethane anaesthesia. Injections of 6-OHDA into the medial forebrain bundle, which depleted noradrenaline and adrenaline in the hypothalamus, lowered basal blood pressure but potentiated the pressor responses to stimulation. In contrast, intraspinal injection of 6-OHDA raised basal blood pressure and attenuated pressor responses. This was accompanied by a partial depletion of adrenaline and the almost complete disappearance of noradrenaline in the spinal cord. Thus, the attenuation of pressor responses observed previously following icvt 6-OHDA can be attributed to an effect on spinal CA pathways. The effects on basal blood pressure suggest that, in SHR, ascending CA pathways are tonically pressor, while spinal CA pathways are depressor. Whilst it is unlikely, therefore, that spinal CAs mediate vasomotor outflow, the altered responses to stimulation after 6-OHDA suggest that central CA pathways can modulate the sensitivity of vasomotor neurones

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