Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Microinjections of norepinephrine within the superficial laminae of trigeminal subnucleus caudalis evoke increases in plasma adrenocorticotropin in the rat. 166 15

In normal male volunteers, intravenous infusions of the alpha 1-adrenergic agonist methoxamine stimulated the secretion of prolactin, thyroid-stimulating hormone (TSH), and adrenocorticotropic hormone (ACTH), and the effects were abolished by pretreatment with the alpha 1-antagonist prazosin. To investigate the site of action of methoxamine, its effects were compared with those of equipotent doses of norepinephrine, an alpha 1-agonist that reaches the pituitary gland and the median eminence after an intravenous infusion but, unlike methoxamine, does not cross the blood-brain barrier. Norepinephrine did not stimulate secretion of prolactin, TSH, or ACTH, suggesting that the stimulant alpha 1-adrenoceptors are located in the central nervous system and not directly on the pituitary gland or in the periphery. The alpha 2- and beta-adrenoceptor agonist properties of norepinephrine could not account for the differences from methoxamine, as pretreatment with prazosin did not modify hormone concentrations after norepinephrine. Methoxamine had no behavioral stimulant effects, as judged by visual analog scales that were sensitive to physiological changes in behavioral arousal. In four patients with hypothalamic dysfunction but responsive pituitary corticotrophs, methoxamine had no stimulant effect on the secretion of ACTH, confirming that the alpha 1-adrenoceptors that stimulate ACTH secretion are not located directly on the pituitary. None of the drugs had an effect on the secretion of growth hormone or the gonadotrophins.
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PMID:Activation of central alpha 1-adrenoceptors in humans stimulates secretion of prolactin and TSH, as well as ACTH. 838 37