Li J, Bukoski R D
Division of General Internal Medicine, University of Texas Medical Branch, Galveston 77550.
Circ Res. 1993 Feb;72(2):290-6. doi: 10.1161/01.res.72.2.290.
Endothelium-dependent relaxation of mesenteric resistance arteries of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats was studied. Acetylcholine-induced relaxation of SHR vessels precontracted with 10 microM norepinephrine was endothelium dependent and attenuated compared with WKY vessels. The impaired response of SHR vessels was normalized by inhibition of cyclooxygenase with indomethacin. Blockade of nitric oxide synthetase with NG-nitro L-arginine methyl ester (L-NAME) or inhibition of guanylate cyclase with methylene blue attenuated acetylcholine-induced relaxation of norepinephrine-contracted SHR vessels but had no effect on WKY vessels. When vessels were precontracted with 30 nM arginine vasopressin, acetylcholine induced similar degrees of relaxation in both strains. A similar response was detected when lysine vasopressin was used to induce tone. Indomethacin had no effect on relaxation responses of SHR and WKY vessels precontracted with either form of vasopressin. L-NAME and methylene blue partially inhibited acetylcholine-induced relaxation of vasopressin-contracted vessels from both strains. Acetylcholine added at baseline did not induce contraction of vessels from either strain. It is concluded that endothelium-dependent relaxation of SHR resistance arteries is not impaired under all circumstances. Acetylcholine-induced relaxation may be suppressed in SHR resistance arteries when norepinephrine is used to induce contraction as a result of catecholamine-induced production of an endothelium-derived contracting factor. Vasopressin, on the other hand, does not elicit production of this contracting factor and may enhance the vasorelaxant action of acetylcholine in resistance arteries of both strains via actions on endothelial or vascular smooth muscle cells.
研究了自发性高血压大鼠（SHR）和正常血压的Wistar-Kyoto（WKY）大鼠肠系膜阻力动脉的内皮依赖性舒张。用10微摩尔去甲肾上腺素预收缩的SHR血管，乙酰胆碱诱导的舒张是内皮依赖性的，与WKY血管相比有所减弱。用吲哚美辛抑制环氧化酶可使SHR血管受损的反应恢复正常。用NG-硝基-L-精氨酸甲酯（L-NAME）阻断一氧化氮合酶或用亚甲蓝抑制鸟苷酸环化酶可减弱乙酰胆碱诱导的去甲肾上腺素预收缩的SHR血管的舒张，但对WKY血管无影响。当血管用30纳摩尔精氨酸加压素预收缩时，乙酰胆碱在两种品系中诱导的舒张程度相似。当用赖氨酸加压素诱导张力时，检测到类似的反应。吲哚美辛对用任何一种加压素预收缩的SHR和WKY血管的舒张反应均无影响。L-NAME和亚甲蓝部分抑制乙酰胆碱诱导的两种品系加压素预收缩血管的舒张。在基线时添加乙酰胆碱不会诱导两种品系血管的收缩。结论是，SHR阻力动脉的内皮依赖性舒张并非在所有情况下都受损。当用去甲肾上腺素诱导收缩时，由于儿茶酚胺诱导产生内皮源性收缩因子，乙酰胆碱诱导的SHR阻力动脉舒张可能受到抑制。另一方面，加压素不会引发这种收缩因子的产生，并且可能通过作用于内皮或血管平滑肌细胞增强两种品系阻力动脉中乙酰胆碱的血管舒张作用。
