Contraction of diabetic rabbit aorta caused by endothelium-derived PGH2-TxA2

摘要: Endothelium-dependent relaxations and vasoactive prostanoid production caused by acetylcholine were determined in the aortas of rabbits with diabetes mellitus induced alloxan. Aortas diabetic rabbits, contracted submaximally phenylephrine, showed significantly decreased endothelium-dependent compared normal rabbits. Indomethacin, a cyclooxygenase inhibitor, SQ 29548, prostaglandin H2-thromboxane A2 (PGH2-TxA2) receptor antagonist, normalized sensitivity to acetylcholine, whereas these agents had no effect on response aortas. The nonreceptor-mediated vasodilator, A23187, an endothelium-independent sodium nitroprusside, not different between Acetylcholine also contractions resting aortic rings endothelium from diabetic, but rabbits; inhibited indomethacin. Synthesis TxA2, measured as immunoreactive TxB2, was increased segments only when present. These results suggest that state, releases major vasoconstrictor product either directly counteracts relaxation or selectively interferes release endothelium-derived relaxing factor(s) cholinergic stimulation. is most likely TxA2 possibly its precursor, PGH2.