Prostacyclin and thromboxane production of rat and cat arterial tissue is altered independently by several vasoactive substances.
The modulation of the production of prostacyclin and thromboxane from cat and cat aortic tissue slices by different vasoactive agents has been studied in order to reveal whether the release of these main two vasoactive prostanoids goes in parallel or may be controlled independently. Norepinephrine, isoproterenol, phentolamine, propranolol, angiotensin II, vasopressin, bradykinin, thrombin, verapamil, gallopamil, dopamine or methionin enkephalin were added to the incubation medium and 6-keto-PGF1 alpha (the stable metabolite of prostacyclin) and TxB2 (the stable metabolite of thromboxane) were determined in the supernatant by radioimmunoassay. The ratio of the release of prostacyclin and thromboxane was computed. Norepinephrine increased both prostacyclin and thromboxane release. Isoproterenol increased the ratio of prostacyclin and thromboxane released in cat aortic tissue slices. Phentolamine and propranolol had no effects. Angiotensin II induced a slight but statistically insignificant increase in the ratio of the two prostanoids released. Vasopressin increased thromboxane release only. Bradykinin stimulated the prostacyclin while thrombin stimulated the thromboxane release. Verapamil decreased both prostacyclin and thromboxane production. Gallopamil decreased prostacyclin release and increased thromboxane release from vessel wall slices in a certain concentration range causing a characteristic dose dependent minimum in the ratio of prostacyclin and thromboxane release. Dopamine separately increased prostacyclin release while enkephalin had no significant effect. The data obtained show that in vascular tissue some unidentified yet cytophysiological mechanisms might exist which specifically control the activities of the prostacyclin synthase and thromboxane synthase enzymes.
Szekacs
B
B
2nd Clinics of Internal Medicine, Semmelweis University of Medicine, Budapest, Hungary.
Nadasy
G L
GL
Vajo
Z
Z
Juhasz
I
I
Feher
J
J
Monos
E
E
D015121:6-Ketoprostaglandin F1 alpha / Q000378:metabolism; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001011:Aorta / Q000187:drug effects* / Q000378:metabolism*; D001920:Bradykinin / Q000494:pharmacology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002316:Cardiotonic Agents / Q000494:pharmacology; D002415:Cats; D004298:Dopamine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D011464:Epoprostenol / Q000096:biosynthesis* / Q000378:metabolism; D005711:Gallopamil / Q000494:pharmacology; D007545:Isoproterenol / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010646:Phentolamine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D051381:Rats; D013917:Thrombin / Q000494:pharmacology; D013929:Thromboxane B2 / Q000096:biosynthesis* / Q000378:metabolism; D014662:Vasoconstrictor Agents / Q000494:pharmacology*; D014665:Vasodilator Agents / Q000494:pharmacology; D014667:Vasopressins / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
D000959:Antihypertensive Agents; D002121:Calcium Channel Blockers; D002316:Cardiotonic Agents; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D014667:Vasopressins; D000804:Angiotensin II; D005711:Gallopamil; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; D011433:Propranolol; D014700:Verapamil; D011464:Epoprostenol; D013917:Thrombin; D007545:Isoproterenol; D001920:Bradykinin; D004298:Dopamine; D009638:Norepinephrine; D010646:Phentolamine