Catecholamines mediate nicotine-induced adrenocorticotropin secretion via α-adrenergic receptors

Shannon G. Matta, Jasbir Singh, Burt Sharp

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Previous studies determined that iv nicotine stimulates ACTH secretion by acting on sites accessible from the fourth ventricle (IV), rather than directly on CRF-containing neurons in the hypothalamus. Brainstem catecholaminergic cell groups, which are accessible from the IV, project to the hypothalamus catecholamines in nicotine-stimulated ACTH secretion. Experiments with the catecholaminergic neurotoxin, 6-hydroxydopamine, demonstrate that the ACTH response to nicotine delivered iv (0.03 or 0.05 mg/kg body wt) or instilled into the IV (1 or 2.5 μg) was significantly reduced in lesioned animals (P < 0.01). Selective inhibitors of epinephrine synthesis, SKF 64139 and 2, 3-dichloro-α- methylbenzylamine (DCMB), significantly reduced (P < 0.01) the ACTH response to 0.05 mg/kg body wt nicotine iv, without affecting median eminence CRF content. Because controversy exists about the effect of DCMB as an α2 adrenoreceptor antagonist in vivo, this was examined by administering norepinephrine into the third ventricle after DCMB ip; DCMB significantly reduced the ACTH response to norepinephrine 0.2 μg (P < 0.05) but not to 0.5 /μg. To determine whether α2 receptors are indeed involved in the ACTH response to nicotine, yohimbine, an α2 antagonist, was injected into the third ventricle before nicotine injection into the IV. Yohimbine significantly reduced the ACTH response. Thus, the secretion of both hypothalamic epinephrine and, to some extent, norepinephrine is involved in the ACTH response to the activation of catecholaminergic neurons in the IV. Further investigation of the adrenergic receptor(s) involved compared the ACTH response to nicotine (1 μg) instilled into the IV after prazocin (α1 antagonist), or propranolol (β antagonist) was injected into the third ventricle. Prazocin significantly reduced (P < 0.05) the ACTH response, whereas propranolol was ineffective. Thus, both α1 and α2 receptors are involved in mediating the ACTH response to nicotine.

Original languageEnglish (US)
Pages (from-to)1646-1655
Number of pages10
JournalEndocrinology
Volume127
Issue number4
DOIs
StatePublished - Jan 1 1990

Fingerprint

Nicotine
Adrenocorticotropic Hormone
Adrenergic Receptors
Catecholamines
Third Ventricle
Norepinephrine
Yohimbine
Propranolol
Epinephrine
Hypothalamus
Neurons
Fourth Ventricle
Median Eminence
Oxidopamine
Neurotoxins
Brain Stem
Injections

All Science Journal Classification (ASJC) codes

  • Endocrinology

Cite this

Catecholamines mediate nicotine-induced adrenocorticotropin secretion via α-adrenergic receptors. / Matta, Shannon G.; Singh, Jasbir; Sharp, Burt.

In: Endocrinology, Vol. 127, No. 4, 01.01.1990, p. 1646-1655.

Research output: Contribution to journalArticle

Matta, Shannon G. ; Singh, Jasbir ; Sharp, Burt. / Catecholamines mediate nicotine-induced adrenocorticotropin secretion via α-adrenergic receptors. In: Endocrinology. 1990 ; Vol. 127, No. 4. pp. 1646-1655.
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abstract = "Previous studies determined that iv nicotine stimulates ACTH secretion by acting on sites accessible from the fourth ventricle (IV), rather than directly on CRF-containing neurons in the hypothalamus. Brainstem catecholaminergic cell groups, which are accessible from the IV, project to the hypothalamus catecholamines in nicotine-stimulated ACTH secretion. Experiments with the catecholaminergic neurotoxin, 6-hydroxydopamine, demonstrate that the ACTH response to nicotine delivered iv (0.03 or 0.05 mg/kg body wt) or instilled into the IV (1 or 2.5 μg) was significantly reduced in lesioned animals (P < 0.01). Selective inhibitors of epinephrine synthesis, SKF 64139 and 2, 3-dichloro-α- methylbenzylamine (DCMB), significantly reduced (P < 0.01) the ACTH response to 0.05 mg/kg body wt nicotine iv, without affecting median eminence CRF content. Because controversy exists about the effect of DCMB as an α2 adrenoreceptor antagonist in vivo, this was examined by administering norepinephrine into the third ventricle after DCMB ip; DCMB significantly reduced the ACTH response to norepinephrine 0.2 μg (P < 0.05) but not to 0.5 /μg. To determine whether α2 receptors are indeed involved in the ACTH response to nicotine, yohimbine, an α2 antagonist, was injected into the third ventricle before nicotine injection into the IV. Yohimbine significantly reduced the ACTH response. Thus, the secretion of both hypothalamic epinephrine and, to some extent, norepinephrine is involved in the ACTH response to the activation of catecholaminergic neurons in the IV. Further investigation of the adrenergic receptor(s) involved compared the ACTH response to nicotine (1 μg) instilled into the IV after prazocin (α1 antagonist), or propranolol (β antagonist) was injected into the third ventricle. Prazocin significantly reduced (P < 0.05) the ACTH response, whereas propranolol was ineffective. Thus, both α1 and α2 receptors are involved in mediating the ACTH response to nicotine.",
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