title: Pharmacological modulation of prostacyclin and thromboxane production of rat and cat venous tissue slices.
abstract: To reveal a potential modulating effect of vasoactive pharmacological agents on the prostanoid production of the venous wall, prostacyclin and thromboxane release from venous tissue slices was studied. Aortic and caval vein samples from 20 rats as well as from 21 cats were studied. Prostacyclin and thromboxane productions were determined by radioimmunoassay as 6-keto-PGF1 alpha and TxB2 released into the incubation medium. Venous tissue produced significantly less prostacyclin per unit weight than arterial tissue in rats (30.7 +/- 4.6 vs. 52.1 +/- 8.2 pg/mg/min), while in cats an opposite situation was found (16.6 +/- 3.2 vs. 7.06 +/- 1.9 pg/mg/min). Thromboxane production of venous tissue was consequently higher than corresponding values for aortic tissue (3.72 +/- 0.46 vs. 1.54 +/- 0.14 in rats and 3.4 +/- 0.6 vs. 1.33 +/- 0.19 in cats, all values in pg/mg/min). Norepinephrine and dopamine significantly increased both the prostacyclin and the thromboxane release from venous tissue, while isoproterenol had no effect. Vasopressin significantly increased thromboxane release and decreased the ratio of prostacyclin vs. thromboxane production (from 10.4 +/- 1.6 to 7.5 +/- 1.6, in acetylsalicylic acid pretreated cats). Angiotensin and thrombin had no significant effects. Bradykinin (0.5 microgram/ml) significantly augmented prostacyclin release from venous tissue (14.4 +/- 2.6 from 10.9 +/- 2.4 pg/mg/min) and decreased thromboxane release (0.65 +/- 0.18 from 1.35 +/- 0.22 pg/mg/min). Methionine-enkephalin (5 micrograms/ml) significantly reduced the thromboxane release from venous tissue slices. The presented material demonstrates that several vasoactive agents modulate the vasoactive prostanoid release of the venous wall. In some cases, the prostacyclin and the thromboxane productions are influenced separately, which in turn will have its impact on smooth muscle activity and thrombocyte aggregation.
authors.affiliation: Experimental Research Institute, Semmelweis University of Medicine, Budapest, Hungary.
authors.forename: G L
authors.initials: GL
authors.lastname: Nadasy
authors.forename: B
authors.initials: B
authors.lastname: Szekacs
authors.forename: I
authors.initials: I
authors.lastname: Juhasz
authors.forename: E
authors.initials: E
authors.lastname: Monos
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000096:biosynthesis*; D000818:Animals; D001011:Aorta / Q000187:drug effects / Q000378:metabolism; D001920:Bradykinin / Q000494:pharmacology; D002415:Cats; D004298:Dopamine / Q000494:pharmacology; D004744:Enkephalin, Methionine / Q000494:pharmacology; D005260:Female; D007545:Isoproterenol / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D013929:Thromboxane B2 / Q000096:biosynthesis*; D014680:Veins / Q000187:drug effects* / Q000378:metabolism*; D014684:Venae Cavae / Q000187:drug effects / Q000378:metabolism; D014700:Verapamil / Q000494:pharmacology
chemical_list: D013929:Thromboxane B2; D004744:Enkephalin, Methionine; D015121:6-Ketoprostaglandin F1 alpha; D014700:Verapamil; D007545:Isoproterenol; D001920:Bradykinin; D004298:Dopamine; D009638:Norepinephrine