ACTIVATION OF THROMBOXANE RECEPTORS AND THE INDUCTION OF VASOMOTION IN THE HAMSTER-CHEEK POUCH MICROCIRCULATION

1 The present study was designed to investigate a possible role of thr omboxane A(2) (TXA(2)) on arteriolar vasomotion (spontaneous rhythmic variations of the vessel diameter). Therefore the microcirculatory eff ects of the thromboxane-receptor (TP-receptor) agonist, U 46619, as we ll as the effects of the TP-receptor antagonists S 17733 and Bay U3405 were evaluated in the hamster cheek pouch microcirculation. For compa rison some effects of angiotensin II were also investigated. 2 For mic rocirculatory measurements, the cheek pouch preparation was placed und er an intravital microscope coupled to a closed circuit TV system. The TV monitor display was used to obtain arteriolar internal diameter me asurements by means of an image shearing device. 3 Superfusion (0.1 nM to 1 mu M) or bolus application (1 pmol to 10 nmol) of U 46619 concen tration-or dose-dependently decreased the arteriolar diameter and indu ced vasomotion in arterioles with a mean initial diameter of 24+/-2 mu m. Both the vasoconstriction and the vasomotion induced by U 46619 we re inhibited by the TP-receptor antagonists S 17733 (100 mg kg(-1), i. v.) and Bay U3405 (10 mg kg(-1), i.v.). 4 Bolus applications of angiot ensin II (0.1 pmol to 1 nmol) induced transient vasoconstriction follo wed by vasodilatation in the cheek pouch arterioles. The dilatation bu t not the constriction, was sensitive to treatment with the NO-synthas e inhibitor N-omega-nitro-L-arginine (L-NOARG; 100 mu M). Angiotensin II did not induce vasomotion in control conditions or in the presence of L-NOARG. 5 Bolus application of phenylephrine (10 pmol) induced vas oconstriction but no vasomotion in previously quiescent hamster cheek pouch arterioles. 6 These results indicate that activation of TP-recep tors causes vasomotion in the hamster cheek pouch arterioles. These sp ontaneous rhythmic variations in arteriolar diameter are not observed with equipotent doses of angiotensin II and phenylephrine. Thus, the v asoconstriction by itself cannot explain the occurrence of vasomotion observed with the TP-receptor agonist.