title: Histamine actions in dog retinal central arteries as compared to those in middle cerebral and temporal arteries.
abstract: OBJECTIVE
  Mechanisms underlying the relaxant response to histamine were compared in isolated dog retinal arteries (branch of internal and external carotid arteries), middle cerebral arteries (branch of internal carotid artery) and superficial temporal arteries (branch of external carotid artery).
  
  
  METHODS
  Changes in the isometric tension of helical strips of the arteries with and without the endothelium were recorded.
  
  
  RESULTS
  Histamine produced concentration-related biphasic (phasic and sustained) relaxations in retinal arterial strips contracted partially with prostaglandin (PG)F2 alpha. Relaxations induced by histamine were not dependent on the endothelium. Treatment with cimetidine attenuated the sustained relaxation, whereas chlorpheniramine or indomethacin depressed the phasic relaxation. In addition, the phasic relaxant response to histamine was attenuated by tranylcypromine, a PGI2 synthesis inhibitor. In contrast, the amine-induced relaxant responses in dog middle cerebral arterial branch and temporal arteries were markedly suppressed by cimetidine alone.
  
  
  CONCLUSIONS
  In dog retinal arteries, the phasic relaxation caused by histamine is mediated by PGI2 in association with activation of the H1 receptor subtype in subendothelial tissues, possibly smooth muscle, and the sustained relaxation is evoked by direct stimulation of the H2 receptor subtype in smooth muscle. The histamine-induced relaxation in temporal and distal middle cerebral arteries is associated solely with a stimulation of H2 receptors in smooth muscle.
authors.affiliation: Department of Pharmacology, Shiga University of Medical Sciences, Seta, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Kitamura
authors.forename: T
authors.initials: T
authors.lastname: Okamura
authors.forename: K
authors.initials: K
authors.lastname: Kani
authors.forename: N
authors.initials: N
authors.lastname: Toda
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology; D002536:Cerebral Arteries / Q000187:drug effects* / Q000502:physiology; D002744:Chlorpheniramine / Q000494:pharmacology; D002927:Cimetidine / Q000494:pharmacology; D015237:Dinoprost / Q000494:pharmacology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology; D011464:Epoprostenol / Q000502:physiology; D005260:Female; D006632:Histamine / Q000494:pharmacology*; D006634:Histamine H1 Antagonists / Q000494:pharmacology; D006635:Histamine H2 Antagonists / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D011969:Receptors, Histamine H1 / Q000378:metabolism; D011970:Receptors, Histamine H2 / Q000378:metabolism; D012161:Retinal Artery / Q000187:drug effects* / Q000502:physiology; D013373:Substance P / Q000494:pharmacology; D013699:Temporal Arteries / Q000187:drug effects* / Q000502:physiology
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D006634:Histamine H1 Antagonists; D006635:Histamine H2 Antagonists; D011969:Receptors, Histamine H1; D011970:Receptors, Histamine H2; D013373:Substance P; D002744:Chlorpheniramine; D002927:Cimetidine; D006632:Histamine; D015237:Dinoprost; D011464:Epoprostenol; D007213:Indomethacin