Microinjections of norepinephrine within the superficial laminae of trigeminal subnucleus caudalis evoke increases in plasma adrenocorticotropin in the rat.

To determine if local release of norepinephrine within the medullary dorsal horn influences autonomic responses often associated with nociception, microinjections of norepinephrine or of specific adrenergic receptor agonists were directed at the trigeminal subnucleus caudalis (Vc) in pentobarbital-anesthetized rats. Norepinephrine (20 nmol, 100 nl) evoked a significant increase (+ 233.8 +/- 89.5 pg/ml, P less than 0.01) in plasma concentrations of adrenocorticotropin (ACTH) after injections within the superficial laminae (I-II) of Vc, whereas mean arterial pressure or heart rate were not affected. Methoxamine (20 nmol), an alpha 1-adrenoceptor agonist, injections into laminae I-II also increased plasma ACTH (+ 90.6 +/- 32 pg/ml, P less than 0.025) without affecting arterial pressure or heart rate. Norepinephrine injections into the deeper laminae (III-V) of Vc caused a variable increase in plasma ACTH (+ 203.5 +/- 146.5 pg/ml, P less than 0.01) that was not mimicked by injections of methoxamine. Microinjections of alpha 2-(clonidine) or beta-(isoproterenol) adrenergic receptor agonists into Vc had no effect on plasma ACTH regardless of the laminar site of injection. The results suggest that norepinephrine acts within Vc to alter selected autonomic responses often associated with nociception. The involvement of an alpha 1-adrenergic receptor subtype within the superficial laminae of the medullary dorsal horn suggests a neural mechanism for norepinephrine-evoked increase in plasma ACTH that is distinct from the well known alpha 2-adrenergic receptor-mediated antinociceptive effects of norepinephrine.