title: Potentiation by hypoxia of contractions caused by angiotensin II in dog and monkey cerebral arteries.
abstract: OBJECTIVE
  Hypoxia alters the responsiveness to endogenous substances of cerebral arteries, possibly resulting in the modulation of blood supply to ischemic brain regions. The present study was undertaken to analyze the mechanism of potentiation by hypoxia of angiotensin II-induced cerebroarterial contractions.
  
  
  METHODS
  Monkey and dog cerebral arterial strips with endothelium were suspended for isometric tension recording in Ringer-Locke solution aerated with 95% O2-5% CO2 (partial pressure, 570-600 mm Hg) or 95% N2-5% CO2 (approximately 10 mm Hg).
  
  
  RESULTS
  Contractions induced by angiotensin II and substance P were potentiated by exposure to hypoxia, whereas contractile responses to prostaglandin F2 alpha were not influenced. Treatment with cyclooxygenase inhibitors abolished the peptide-induced contraction but did not alter the prostaglandin F2 alpha-induced contraction. Relaxations induced by arachidonic acid were suppressed by indomethacin and hypoxia, whereas those caused by a prostaglandin I2 analogue were unaffected.
  
  
  CONCLUSIONS
  The potentiation by hypoxia of cerebroarterial contractions caused by angiotensin II and substance P appears to be due to an interference with the synthesis of prostaglandin I2 from arachidonic acid and a resultant increase in the production of vasoconstrictor prostaglandins.
authors.affiliation: Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Yoshida
authors.forename: T
authors.initials: T
authors.lastname: Okamura
authors.forename: N
authors.initials: N
authors.lastname: Toda
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D002536:Cerebral Arteries / Q000187:drug effects / Q000503:physiopathology*; D003251:Constriction, Pathologic / Q000139:chemically induced / Q000503:physiopathology; D016861:Cyclooxygenase Inhibitors; D015237:Dinoprost / Q000494:pharmacology; D004195:Disease Models, Animal; D004285:Dogs; D004730:Endothelium, Vascular; D005260:Female; D000860:Hypoxia / Q000503:physiopathology*; D008251:Macaca; D008297:Male; D013373:Substance P / Q000494:pharmacology
chemical_list: D016861:Cyclooxygenase Inhibitors; D000804:Angiotensin II; D013373:Substance P; D015237:Dinoprost