title: Plasticity of cardiovascular function in snapping turtle embryos (Chelydra serpentina): chronic hypoxia alters autonomic regulation and gene expression.
abstract: Reptile embryos tolerate large decreases in the concentration of ambient oxygen. However, we do not fully understand the mechanisms that underlie embryonic cardiovascular short- or long-term responses to hypoxia in most species. We therefore measured cardiac growth and function in snapping turtle embryos incubated under normoxic (N21; 21% O₂) or chronic hypoxic conditions (H10; 10% O₂). We determined heart rate (fH) and mean arterial pressure (Pm) in acute normoxic (21% O₂) and acute hypoxic (10% O₂) conditions, as well as embryonic responses to cholinergic, adrenergic, and ganglionic pharmacological blockade. Compared with N21 embryos, chronic H10 embryos had smaller bodies and relatively larger hearts and were hypotensive, tachycardic, and following autonomic neural blockade showed reduced intrinsic fH at 90% of incubation. Unlike other reptile embryos, cholinergic and ganglionic receptor blockade both increased fH. β-Adrenergic receptor blockade with propranolol decreased fH, and α-adrenergic blockade with phentolamine decreased Pm. We also measured cardiac mRNA expression. Cholinergic tone was reduced in H10 embryos, but cholinergic receptor (Chrm2) mRNA levels were unchanged. However, expression of adrenergic receptor mRNA (Adrb1, Adra1a, Adra2c) and growth factor mRNA (Igf1, Igf2, Igf2r, Pdgfb) was lowered in H10 embryos. Hypoxia altered the balance between cholinergic receptors, α-adrenoreceptor and β-adrenoreceptor function, which was reflected in altered intrinsic fH and adrenergic receptor mRNA levels. This is the first study to link gene expression with morphological and cardioregulatory plasticity in a developing reptile embryo.
authors.affiliation: Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA. johneme23@gmail.com
authors.forename: John
authors.initials: J
authors.lastname: Eme
authors.forename: Turk
authors.initials: T
authors.lastname: Rhen
authors.forename: Kevin B
authors.initials: KB
authors.lastname: Tate
authors.forename: Kathryn
authors.initials: K
authors.lastname: Gruchalla
authors.forename: Zachary F
authors.initials: ZF
authors.lastname: Kohl
authors.forename: Christopher E
authors.initials: CE
authors.lastname: Slay
authors.forename: Dane A
authors.initials: DA
authors.lastname: Crossley
mesh_terms: D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000319:Adrenergic beta-Antagonists / Q000494:pharmacology; D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology*; D002320:Cardiovascular Physiological Phenomena; D049033:Chorioallantoic Membrane / Q000502:physiology; D002908:Chronic Disease; D018076:DNA, Complementary / Q000096:biosynthesis / Q000235:genetics; D004625:Embryo, Nonmammalian / Q000502:physiology*; D047108:Embryonic Development / Q000502:physiology; D005730:Ganglionic Blockers / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D010275:Parasympathetic Nervous System / Q000502:physiology; D010276:Parasympatholytics / Q000494:pharmacology; D060888:Real-Time Polymerase Chain Reaction; D017978:Receptors, Growth Factor / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D017981:Receptors, Neurotransmitter / Q000235:genetics; D013564:Sympathetic Nervous System / Q000502:physiology; D014426:Turtles / Q000502:physiology*
chemical_list: D000317:Adrenergic alpha-Antagonists; D000319:Adrenergic beta-Antagonists; D018076:DNA, Complementary; D005730:Ganglionic Blockers; D010276:Parasympatholytics; D017978:Receptors, Growth Factor; D017981:Receptors, Neurotransmitter
keywords: adrenergic tone; cholinergic tone; embryo and fetus; gene expression; hypoxia; reptile