title: Ontogeny of epinephrine metabolic pathways in the rat: role of glucocorticoids.
abstract: Recent studies suggest that the initial expression of adrenal phenylethanolamine N-methyltransferase (PNMT) and epinephrine (E) are dependent upon stimulation of adrenal glucocorticoid receptors. However, evidence suggests that the expression of heart and brain PNMT is independent of glucocorticoids. We measured PNMT activity and E levels in adrenal, heart and head over the latter half of gestation in rat fetuses treated chronically with glucocorticoids, and in normal controls. Chronic glucocorticoid treatment ending on embryonic day (e)12 did not affect heart, head or trunk PNMT activity or E levels. In contrast, chronic glucocorticoid exposure ending e19 or e20 resulted in marked increases in both PNMT and E in adrenal, heart and head tissues. The elevation of E in all three tissues was unaffected by maternal adrenalectomy, indicating enhanced fetal E synthesis. In the absence of exogenous glucocorticoid treatment heart PNMT activity peaked on e12, prior to the earliest reported appearance of glucocorticoid receptors. We conclude that expression of PNMT in all three tissues is glucocorticoid independent until the latter part of gestation when it is readily enhanced by glucocorticoids.
authors.affiliation: Department of Medicine, University of California San Diego, Medical Center, 200 West Arbor Drive, 8341, San Diego, CA, USA. bpkennedy@ucsd.edu
authors.forename: B
authors.initials: B
authors.lastname: Kennedy
authors.forename: M G
authors.initials: MG
authors.lastname: Ziegler
mesh_terms: D000311:Adrenal Glands / Q000737:chemistry / Q000196:embryology / Q000201:enzymology; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000196:embryology* / Q000201:enzymology; D001923:Brain Chemistry / Q000187:drug effects / Q000502:physiology; D002394:Catechol O-Methyltransferase / Q000032:analysis / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology*; D004296:Dopa Decarboxylase / Q000032:analysis / Q000378:metabolism; D015259:Dopamine Agents / Q000494:pharmacology; D004837:Epinephrine / Q000032:analysis / Q000378:metabolism*; D005260:Female; D005333:Fetus / Q000737:chemistry / Q000201:enzymology; D005938:Glucocorticoids / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects / Q000196:embryology*; D007422:Intestines / Q000737:chemistry / Q000196:embryology; D007980:Levodopa / Q000494:pharmacology; D008995:Monoamine Oxidase / Q000032:analysis / Q000378:metabolism; D009206:Myocardium / Q000737:chemistry / Q000201:enzymology; D009638:Norepinephrine / Q000032:analysis / Q000378:metabolism; D010625:Phenylethanolamine N-Methyltransferase / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D011965:Receptors, Glucocorticoid / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis / Q000378:metabolism
chemical_list: D015259:Dopamine Agents; D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D007980:Levodopa; D003907:Dexamethasone; D014446:Tyrosine 3-Monooxygenase; D008995:Monoamine Oxidase; D010625:Phenylethanolamine N-Methyltransferase; D002394:Catechol O-Methyltransferase; D004296:Dopa Decarboxylase; D009638:Norepinephrine; D004837:Epinephrine