title: Beta 2-adrenergic dilation of resistance coronary vessels involves KATP channels and nitric oxide in conscious dogs.
abstract: BACKGROUND
  We considered that beta 2-adrenergic stimulation may dilate resistance coronary vessels by opening ATP-sensitive potassium (KATP) channels, thereby triggering NO formation.
  
  
  RESULTS
  In conscious instrumented dogs after beta 1-adrenergic blockade, intracoronary (IC) injections of acetylcholine (ACh), nitroglycerin (NTG), and pirbuterol (PIR), a selective beta 2-adrenergic agonist, were performed before and after blockade of NO formation with IC N omega-nitro-L-arginine methyl ester (L-NAME, 50 micrograms.kg-1.min-1 x 12 minutes) or blockade of KATP channels with IC glibenclamide (25 micrograms.kg-1.min-1 x 12 minutes followed by 2 micrograms.kg-1.min-1). PIR (50.0 ng/kg) increased coronary blood flow (CBF) by 32 +/- 6 from 43 +/- 7 mL/min and by only 11 +/- 2 (P < .01) from 40 +/- 7 mL/min after L-NAME. Increases in CBF to ACh were also reduced by L-NAME, but NTG responses were not. Before glibenclamide, PIR increased CBF by 33 +/- 5 from 45 +/- 7 mL/min and by only 14 +/- 3 (P < .01) from 36 +/- 5 mL/min thereafter. CBF responses to ACh and NTG were maintained after glibenclamide. Lemakalim, a selective opener of KATP channels, caused dose-dependent increases in CBF that were partially inhibited by L-NAME. In experiments in which CBF was controlled, the fall in distal coronary pressure caused by PIR was less after L-NAME or glibenclamide than before.
  
  
  CONCLUSIONS
  beta 2-Adrenergic dilation of resistance coronary vessels involves both the opening of KATP channels and NO formation. L-NAME antagonized lemakalim responses consistent with a link between the opening of KATP channels and NO formation in canine resistance coronary vessels.
authors.affiliation: Department of Physiology, Faculty of Medicine, Université de Montréal, Québec, Canada.
authors.forename: Z
authors.initials: Z
authors.lastname: Ming
authors.forename: R
authors.initials: R
authors.lastname: Parent
authors.forename: M
authors.initials: M
authors.lastname: Lavallée
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000255:Adenosine Triphosphate / Q000502:physiology*; D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000818:Animals; D001578:Benzopyrans / Q000494:pharmacology; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D019806:Cromakalim; D004285:Dogs; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004983:Ethanolamines / Q000494:pharmacology; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D005996:Nitroglycerin / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D011758:Pyrroles / Q000494:pharmacology; D014655:Vascular Resistance; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D000318:Adrenergic beta-Agonists; D001578:Benzopyrans; D004791:Enzyme Inhibitors; D004983:Ethanolamines; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D011758:Pyrroles; D014665:Vasodilator Agents; D019806:Cromakalim; D009569:Nitric Oxide; D000255:Adenosine Triphosphate; D005996:Nitroglycerin; D000109:Acetylcholine; C009118:pirbuterol; D019331:NG-Nitroarginine Methyl Ester