Role of adrenaline neurons of ventrolateral medulla (the C1 group) in the tonic and phasic control of arterial pressure.

Abstract

We have sought to determine if adrenaline neurons of the C1 group are responsible for cardiovascular functions heretofore attributed to neurons in the rostral ventrolateral medulla. C1 neurons were identified in rat with antibodies to the adrenaline synthesizing enzyme, PNMT. These project to spinal cord wherein they selectively innervate the sympathetic columns. C1 neurons are also innervated by projections, mostly unilateral, from the nucleus tractus solitarii (NTS). Stimulation of the C1 area electrically, by local injection of the excitatory amino acid, L-glutamate, or with the GABA antagonist bicuculline, elevates arterial pressure (AP). Bilateral electrolytic lesions, microinjection of GABA, or administration of tetrodotoxin, in contrast, collapses AP to levels comparable to that of spinal cord transection. After lesions of one NTS, a lesion of the contralateral C1 area abolishes all reflex activity elicited by electrical or natural stimulation of baroreceptors on the side of C1 lesion without modifying resting AP. Lesions of axon bundles of PNMT neurons in the medulla also abolish baroreflexes after unilateral NTS lesions. C1 neurons appear to be the neurons mediating cardiovascular effects of application of drugs or cold to rostral portions of the ventrolateral medulla. We conclude adrenaline neurons of the C1 area represent the purportedly tonic vasomotor neurons of the rostral ventrolateral medulla and mediate the vasodepressor limb of reflexes arising from arterial baroreceptors and other cardiopulmonary afferents. Whether the tonic vasomotor response to stimulation of C1 neurons is dependent upon the release of adrenaline is not yet certain.