Tonic descending inhibition of the spinal somato-sympathetic reflex from the lower brain stem

In chloralose-anaesthetized cats the spinal and supraspinal components of the somato-sympathetic reflex were evoked in the white ramus at T3 and/or L2 by stimulation of intercostal and spinal nerves. A reversible blockade of all ascending and descending spinal pathways was performed by cooling the spinal cord between the second and third cervical segment. Total blockade of conduction was produced at temperatures below 8.5 degrees C (281.5 K). The spinal blockade produced the following reversible effects. (1) Mean arterial pressure fell to 30-50 mm Hg (4.0-6.7 kpa) and the tonic background activity in the white ramus was reduced to 0-24% of control (mean 12.1 +/- 10.0%). (2) The amplitude of the early spinal reflex was increased from 100% to 111-316% (mean 200.9 +/- 49.5%, n = 49) at the thoracic level and to 125-342% (mean 181.4 +/- 74.4%, n = 7) at the lumbar level. The onset latency of the spinal reflex at T3 (range 8-21 msec) was shortened by 0.5-3.0 msec (mean 1.7 +/- 0.9 msec). (3) Supraspinal components were completely abolished. (4) Neither baroreceptor denervation nor midcollicular decerebration altered these effects. (5) The cold block induced increase of the amplitude of the spinal reflex was reduced by the alpha-adrenoceptor agonist clonidine; this effect was reversed by the alpha-adrenoceptor antagonist yohimbine. Selective cooling of the dorsolateral funiculus caused the same effects on the spinal and supraspinal reflexes as cold block of the whole spinal cord. From these findings it is concluded that in the anaesthetized cat the spinal component of the somato-sympathetic reflex is modulated by a descending tonic inhibition. This inhibition acts at both the thoracic and the lumbar level and its origin is in the medulla oblongata. This inhibition is, however, independent of baroreceptor inputs. The pathways descends in the dorsolateral funiculus. It is suggested that noradrenaline or adrenaline might be involved in the transmission of this inhibitory influence.