title: Expression of adrenoceptor subtypes in preterm piglet heart is different to term heart.
abstract: Preterm delivery increases the risk of inadequate systemic blood flow and hypotension, and many preterm infants fail to respond to conventional inotrope treatments. If the profile of cardiac adrenoceptor subtypes in the preterm neonate is different to that at term this may contribute to these clinical problems. This study measured mRNA expression of β1, β2, α1A, α2A and α2B-adrenoceptor subtypes by real time PCR in term (113d), preterm (91d) and preterm piglets (91d) exposed to maternal glucocorticoid treatment. Abundance of β-adrenoceptor binding sites in the left ventricle was measured using saturation binding assays. Relative abundance of β1-adrenoceptor mRNA in untreated preterm hearts was ∼50% of term abundance in both left and right ventricles (P<0.001). Trends in receptor binding site density measurements supported this observation (P = 0.07). Glucocorticoid exposure increased β1-adrenoceptor mRNA levels in the right ventricle of preterm hearts (P = 0.008) but did not alter expression in the left ventricle (P>0.1). Relative abundance of α1A-adrenoceptor mRNA was the same in preterm and term piglet hearts (P = >0.1) but was reduced by maternal glucocorticoid treatment (P<0.01); α2A-adrenoceptor mRNA abundance was higher in untreated and glucocorticoid exposed preterm piglet hearts than in term piglets (P<0.001). There was no difference between male and female piglets in mRNA abundance of any of the genes studied. In conclusion, there is reduced mRNA abundance of β1-adrenoceptors in the preterm pig heart. If this lower expression of β-adrenoceptors occurs in human preterm infants, it could explain their poor cardiovascular function and their frequent failure to respond to commonly used inotropes.
authors.affiliation: The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia.
authors.forename: Min Young
authors.initials: MY
authors.lastname: Kim
authors.affiliation: Department of Pharmacology, School of Medical Sciences, The University of New South Wales, Sydney, Australia.
authors.forename: Angela M
authors.initials: AM
authors.lastname: Finch
authors.affiliation: The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia; Department of Physiology, School of Medical Sciences, The University of New South Wales, Sydney, Australia; School of Biomedical Sciences and Pharmacy, University of Newcastle, Newcastle, Australia.
authors.forename: Eugenie R
authors.initials: ER
authors.lastname: Lumbers
authors.affiliation: Department of Physiology, School of Medical Sciences, The University of New South Wales, Sydney, Australia.
authors.forename: Amanda C
authors.initials: AC
authors.lastname: Boyce
authors.affiliation: Department of Physiology, School of Medical Sciences, The University of New South Wales, Sydney, Australia.
authors.forename: Karen J
authors.initials: KJ
authors.lastname: Gibson
authors.affiliation: The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia.
authors.forename: Yvonne A
authors.initials: YA
authors.lastname: Eiby
authors.affiliation: The University of Queensland, UQ Centre for Clinical Research, Brisbane, Australia.
authors.forename: Barbara E
authors.initials: BE
authors.lastname: Lingwood
mesh_terms: D000818:Animals; D001665:Binding Sites; D005260:Female; D018507:Gene Expression Regulation, Developmental; D006321:Heart / Q000196:embryology*; D008297:Male; D009206:Myocardium / Q000378:metabolism; D047928:Premature Birth / Q000378:metabolism*; D011941:Receptors, Adrenergic / Q000235:genetics / Q000378:metabolism*; D011942:Receptors, Adrenergic, alpha / Q000235:genetics / Q000378:metabolism; D011943:Receptors, Adrenergic, beta / Q000235:genetics / Q000378:metabolism; D034421:Sus scrofa / Q000196:embryology*; D047929:Term Birth / Q000378:metabolism*
chemical_list: D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D011943:Receptors, Adrenergic, beta