title: Interaction between prostacyclin and nitric oxide in the reflex control of the coronary circulation in conscious dogs.
abstract: OBJECTIVE
  Our goal was to determine the role of nitric oxide (NO) on the coronary vasodilation induced by prostacyclin (PGI2) in conscious dogs.
  
  
  METHODS
  Dogs were chronically instrumented for the measurements of coronary blood flow (CBF), left ventricular pressure (LVP), mean arterial pressure (MAP) and heart rate (HR).
  
  
  RESULTS
  Intravenous injections of PGI2 caused dose-dependent increases in CBF, and decreases in MAP and late diastolic coronary resistance (LDCR). For instance, CBF increased by 128 +/- 19% (P < 0.05) from 30 +/- 3.5 ml/min and LDCR decreased by 73 +/- 3% (P < 0.05) from 2.57 +/- 0.20 mmHg/ml/min following injection of PGI2 (1.0 microgram/kg). After infusion of nitro-L-arginine (NLA, 35 mg/kg) intravenously, the coronary vasodilation induced by PGI2 was partially attenuated. PGI2 (1.0 microgram/kg) increased CBF by 55 +/- 15% from 33 +/- 5.3 ml/min and decreased LDCR by 42 +/- 9% (both P < 0.05, compared with before NLA) from 3.29 +/- 0.39 mmHg/ml/min. Infusion of L-arginine (100 mg/kg) reversed the action of NLA. For example, PGI2 (1.0 microgram/kg) increased CBF by 115 +/- 15% from 36 +/- 6 ml/min and decreased LDCR by 68 +/- 3% from 3.02 +/- 0.36 mmHg/ml/min (both P > 0.05, compared with before NLA). Atropine (0.1 mg/kg) partially attenuated the coronary vasodilation induced by PGI2 the magnitude of which was almost identical to that by NLA. NLA or atropine also blunted the coronary vasodilation induced by acetylcholine, while the coronary vasodilation induced by nitroglycerin was not affected by NLA.
  
  
  CONCLUSIONS
  Our results indicate that the coronary vasodilation induced by PGI2 was partially attenuated by NLA or atropine, suggesting that the coronary vasodilation induced by PGI2 is due to two components: a reflex parasympathetic cholinergic vasodilation mediated by NO and a direct action of PGI2.
authors.affiliation: Department of Physiology, New York Medical College, Valhalla 10595, USA.
authors.forename: G
authors.initials: G
authors.lastname: Zhao
authors.forename: X
authors.initials: X
authors.lastname: Xu
authors.forename: M
authors.initials: M
authors.lastname: Ochoa
authors.forename: W
authors.initials: W
authors.lastname: Shen
authors.forename: T H
authors.initials: TH
authors.lastname: Hintze
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D003326:Coronary Circulation / Q000187:drug effects*; D004285:Dogs; D011464:Epoprostenol / Q000494:pharmacology*; D007213:Indomethacin / Q000494:pharmacology; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D005996:Nitroglycerin / Q000494:pharmacology; D010276:Parasympatholytics / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011448:Prostaglandin Antagonists / Q000494:pharmacology; D012018:Reflex / Q000187:drug effects*; D013565:Sympatholytics / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D014666:Vasomotor System / Q000187:drug effects*
chemical_list: D010276:Parasympatholytics; D011448:Prostaglandin Antagonists; D013565:Sympatholytics; D014665:Vasodilator Agents; D019335:Nitroarginine; D009569:Nitric Oxide; D001285:Atropine; D011433:Propranolol; D011464:Epoprostenol; D019001:Nitric Oxide Synthase; D005996:Nitroglycerin; D000109:Acetylcholine; D007213:Indomethacin