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Possible involvement of prostaglandins in vasoconstriction induced by zymosan and arachidonic acid in the perfused rat liver
Author(s) -
Dieter Peter,
Altin Joseph.G.,
Bygrave Fyfe L.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)81486-2
Subject(s) - nordihydroguaiaretic acid , arachidonic acid , vasoconstriction , zymosan , phenylephrine , chemistry , hypoxic pulmonary vasoconstriction , cyclooxygenase , prostaglandin , endocrinology , lipoxygenase , pharmacology , medicine , biochemistry , biology , blood pressure , enzyme , in vitro
Exposure of perfused livers to zymosan, arachidonic acid or phenylephrine but not to latex particles, stimulates hepatic constriction. The effects of arachidonic acid are rapid, reach a maximum after 2–3 min and then decline. They are blocked by the cyclooxygenase inhibitor indomethacin but not by the lipoxygenase inhibitor nordihydroguaiaretic acid. This suggests a role for prostaglandins in this action. Zymosan progressively increases hepatic pressure after a lag time of about 1 min. Perfusion of bromophenacyl bromide, indomethacin and nordihydroguaiaretic acid only partially inhibits the zymosan‐induced vasoconstriction. None of these inhibitors affect the phenylephrine‐induced response. Repeated infusion of arachidonic acid leads to homologous desensitization of the response whereas the response of the liver to phenylephrine is unaffected. The present data indicate that prostaglandins, produced and released within the liver, affect vasoconstriction in this organ.