title: Intrapulmonary arteries respond to serotonin and adenosine triphosphate in broiler chickens susceptible to idiopathic pulmonary arterial hypertension.
abstract: This study examined factors contributing to increased vascular resistance and plexiform lesion formation in broiler chickens susceptible to idiopathic pulmonary arterial hypertension (IPAH). A diet supplemented with excess tryptophan (high-Trp diet), the precursor for serotonin, was used to accelerate the development of IPAH. Broilers fed the high-Trp diet had higher pulmonary arterial pressures than broilers fed the control diet, and plexiform lesion incidences tended to be higher (P = 0.11) in the high-Trp group than in the control group at 30 d of age. The intrapulmonary arteries were assessed for vasoconstriction in response to serotonin and adenosine triphosphate (ATP) and for activities of key metabolic enzymes for serotonin and ATP. The pulmonary artery (defined as the first major branch of the pulmonary artery inside the lung) and the primary pulmonary arterial rami (defined as the second major branch of the pulmonary artery inside the lung) both exhibited vasoconstriction in response to serotonin and ATP. This is the first study to demonstrate purinergic-mediated vasoconstriction in intrapulmonary arteries from broilers. Arteriole responsiveness did not differ between broilers fed the control diet or the high-Trp diet. Therefore, the high-Trp diet enhanced the development of IPAH but did not affect the artery's sensitivity to serotonin or ATP. Monoamine oxidase activity, responsible for the breakdown of serotonin, was severely impaired in pulmonary arteries from broilers in the high-Trp group. Accordingly, serotonin may persist longer and elicit an amplified response in broilers fed the high-Trp diet.
authors.affiliation: Department of Kinesiology, Auburn University, AL 36849, USA. hak0006@auburn.edu
authors.forename: H A
authors.initials: HA
authors.lastname: Kluess
authors.forename: J
authors.initials: J
authors.lastname: Stafford
authors.forename: K W
authors.initials: KW
authors.lastname: Evanson
authors.forename: A J
authors.initials: AJ
authors.lastname: Stone
authors.forename: J
authors.initials: J
authors.lastname: Worley
authors.forename: R F
authors.initials: RF
authors.lastname: Wideman
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001160:Arterioles / Q000473:pathology / Q000503:physiopathology; D002645:Chickens; D019587:Dietary Supplements / Q000032:analysis; D004198:Disease Susceptibility / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology; D065627:Familial Primary Pulmonary Hypertension; D006976:Hypertension, Pulmonary / Q000139:chemically induced / Q000473:pathology* / Q000503:physiopathology; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D008297:Male; D008995:Monoamine Oxidase / Q000378:metabolism; D010744:Phosphoric Monoester Hydrolases / Q000378:metabolism; D011651:Pulmonary Artery / Q000473:pathology* / Q000503:physiopathology; D012701:Serotonin / Q000378:metabolism*; D014364:Tryptophan / Q000008:administration & dosage / Q000494:pharmacology*; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000378:metabolism*
chemical_list: D014662:Vasoconstrictor Agents; D012701:Serotonin; D014364:Tryptophan; D000255:Adenosine Triphosphate; D008995:Monoamine Oxidase; D010744:Phosphoric Monoester Hydrolases