title: Steady state levels of hepatic alpha 1- and beta 2-adrenergic receptors and gene transcripts during development of the male rat.
abstract: Metabolic events stimulated by epinephrine and norepinephrine in hepatocytes isolated from fetal and early postnatal male rats are largely mediated through the beta 2-adrenergic receptor-/cyclic AMP dependent-system, whereas the same stimuli are transduced through the alpha 1-adrenergic receptor-/phosphatidylinositol dependent-system in hepatocytes isolated from young adult male rats. This developmental transition was investigated by correlating hepatic alpha 1- and beta 2-adrenergic receptor gene transcript levels with receptor levels as determined with selective radioligands in livers from late fetal to postnatal day 120 male Sprague-Dawley rats. beta 2-Adrenergic receptor concentration, initially high in membrane preparations isolated from fetal livers (203 +/- 21 fmol/mg protein), dropped precipitously in postnatal day 6 livers (14 +/- 2 fmol/mg protein) and remained low throughout development out to postnatal day 90. beta 2-Adrenergic receptor mRNA levels were highest in fetal livers, were decreased somewhat in postnatal day 6 livers and were undetectable in livers beyond postnatal day 15. In contrast, hepatic alpha 1-adrenergic receptor concentration was relatively low in fetal livers (86 +/- 25 fmol/mg protein) and remained low until postnatal day 18. Thereafter, a steady increase in alpha 1-adrenergic receptors was observed until adult levels. (270 +/- 24 fmol/mg protein) were achieved at postnatal day 27. alpha 1-Adrenergic receptor mRNA levels increased approximately 3-fold, reaching a peak at postnatal day 24. Surprisingly, at postnatal day 30 hepatic alpha 1-adrenergic receptor mRNA levels dropped to fetal levels; but, gradually increased with continued development. Thus, hepatic alpha 1- and beta 2-adrenergic receptors appear to be under complex regulatory control which may include transcriptional, as well as post-transcriptional, mechanisms.
authors.affiliation: Department of Physiology and Biophysics, University of Arkansas for Medical Sciences, Little Rock 72205-7199.
authors.forename: S P
authors.initials: SP
authors.lastname: Rossby
authors.forename: L E
authors.initials: LE
authors.lastname: Cornett
mesh_terms: D000367:Age Factors; D000818:Animals; D015152:Blotting, Northern; D015870:Gene Expression; D008099:Liver / Q000502:physiology*; D008297:Male; D010869:Pindolol / Q000031:analogs & derivatives / Q000378:metabolism; D011224:Prazosin / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics; D051381:Rats; D011942:Receptors, Adrenergic, alpha / Q000235:genetics* / Q000378:metabolism*; D011943:Receptors, Adrenergic, beta / Q000235:genetics* / Q000378:metabolism*
chemical_list: D012333:RNA, Messenger; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta; C047975:cyanopindolol; D010869:Pindolol; D011224:Prazosin