title: Comparison of responses to angiotensin II of dog mesenteric arteries and veins.
abstract: Responses to angiotensin II (AII), arachidonic acid (AA) and prostaglandin (PG) I2 were compared in helical strips of dog mesenteric arteries and veins. Arterial strips contracted in response to AII, whereas venous strips responded with a transient, slight contraction followed by a moderate relaxation. The peptide-induced responses were abolished by treatment with saralasin, but were not influenced by ONO3708, an inhibitor of vasoconstrictor PG actions, or by endothelium denudation. Treatment with indomethacin potentiated the contractile response of the arteries and reversed the relaxant response of veins to a contraction. The concentration of exogenous PGI2 methylester needed to produce a tension development similar to that induced by PGI2 released by AII was greater in the mesenteric arteries than in the veins. The amount of 6-keto PGF1 alpha in the bathing media measured by radioimmunoassay was increased in the arteries and veins stimulated by AII. Exogenously applied PGI2 elicited relaxations of similar magnitude in the arteries and veins. AA-induced relaxations were greater in the veins; indomethacin suppressed the arterial and venous relaxations. The magnitude of the endothelium-dependent relaxation induced by A23187 was similar in the arteries and veins. It appears that the heterogenous responses to AII of dog mesenteric arteries and veins are due mainly to the difference in the AII receptors responsible for smooth muscle contraction and also to the difference in the ability to produce and liberate PGI2. The synthesis and the action of EDRF (endothelium-derived relaxing factor) does not seem to differ in the arteries and veins.
authors.affiliation: Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
authors.forename: M
authors.initials: M
authors.lastname: Yamazaki
authors.forename: N
authors.initials: N
authors.lastname: Toda
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism; D000001:Calcimycin / Q000494:pharmacology; D004285:Dogs; D004730:Endothelium, Vascular / Q000502:physiology; D011464:Epoprostenol / Q000494:pharmacology; D005260:Female; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects*; D008642:Mesenteric Veins / Q000187:drug effects*; D009119:Muscle Contraction / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D009569:Nitric Oxide / Q000502:physiology; D012504:Saralasin / Q000494:pharmacology; D013928:Thromboxane A2 / Q000031:analogs & derivatives / Q000494:pharmacology
chemical_list: D000804:Angiotensin II; D016718:Arachidonic Acid; D009569:Nitric Oxide; D000001:Calcimycin; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; C049855:ONO 3708; D011464:Epoprostenol; D012504:Saralasin; D007213:Indomethacin