title: ATP stimulates the release of prostacyclin from perfused veins isolated from the hamster hindlimb.
abstract: ATP-stimulated prostacyclin release from veins was investigated using epigastric veins isolated from hamsters. Veins were perfused with MOPS-buffered physiological salt solution (PSS). ATP was administered into the perfusate, and the bath solution (MOPS-PSS) was collected and assayed for the presence of the stable prostacyclin metabolite 6-keto-PGF1alpha. ATP (100 microM) resulted in reproducible increases in bath concentration from 73 +/- 22 to 279 +/- 50 pg/ml (P < 0.05, n = 5). This response was abolished by indomethacin (10 microM, P < 0.05). To ascertain whether the endothelium was the source of prostacyclin, endothelium was disrupted using air (n = 10) or deoxycholic acid (n = 6). Perfusion with air significantly reduced (P < 0.05) but did not completely abolish ATP-stimulated release of prostacyclin, while deoxycholic acid totally abolished the response (P < 0.05). The nonselective P2 receptor antagonist reactive blue 2 (100 microM) attenuated ATP-mediated release of prostacyclin but did not significantly alter ACh-stimulated release of prostacyclin. The nonselective adenosine receptor antagonist xanthine amine congener (1 microM) had no effect on ATP-stimulated release, and adenosine did not stimulate the release of prostacyclin. These results show that increases in intraluminal concentration of ATP stimulate abluminal release of prostacyclin from the venous endothelium. This effect is mediated by P2 receptors while adenosine and its receptors are not involved in this response.
authors.affiliation: Dept. of Physiology and Biophysics, Univ. of Mississippi Medical Center, 2500 N. State St., Jackson, MS 39216, USA.
authors.forename: Leah W
authors.initials: LW
authors.lastname: Hammer
authors.forename: Carmen R
authors.initials: CR
authors.lastname: Overstreet
authors.forename: Jaehwa
authors.initials: J
authors.lastname: Choi
authors.forename: Robert L
authors.initials: RL
authors.lastname: Hester
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D006224:Cricetinae; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D006614:Hindlimb; D066298:In Vitro Techniques; D008297:Male; D008647:Mesocricetus; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D058919:Purinergic P2 Receptor Antagonists; D018047:Receptors, Purinergic P1 / Q000378:metabolism; D018048:Receptors, Purinergic P2 / Q000378:metabolism; D014227:Triazines / Q000494:pharmacology; D014680:Veins / Q000187:drug effects* / Q000378:metabolism*
chemical_list: D011500:Protein Synthesis Inhibitors; D058919:Purinergic P2 Receptor Antagonists; D018047:Receptors, Purinergic P1; D018048:Receptors, Purinergic P2; D014227:Triazines; D015121:6-Ketoprostaglandin F1 alpha; C012842:Cibacron Blue F 3GA; D000255:Adenosine Triphosphate; D011464:Epoprostenol