Bansal V, Toga H, Raj J U
Department of Pediatrics, Memorial Medical Center, Long Beach, California.
Respir Physiol. 1993 Aug;93(2):249-60. doi: 10.1016/0034-5687(93)90009-y.
We have determined the role of endogenous nitric oxide (NO) in regulation of vasomotor tone in ovine intrapulmonary and mesenteric vessels with resting tension and elevated vasomotor tone. Third generation intrapulmonary vessel rings and mesenteric vessel rings, 2-3 mm in diameter, were isolated from 20 sheep. NO production in the vessels was assessed by the change in tension induced by NG-nitro-L-arginine methyl ester (L-NAME), a competitive inhibitor of NO synthase. In vessels under resting tension, 10(-4) to 10(-3) M L-NAME induced a significant increase in tension only in veins but not in arteries. When tone was elevated with phenylephrine or U 46,619, a thromboxane A2 analogue, there was now a significant increase in tension in arteries with 10(-4) M L-NAME and in veins with 10(-5) M L-NAME. The increase in tension induced by L-NAME in veins was greater than that in arteries and greater when tone was elevated than under resting tension. Responses of pulmonary and mesenteric vessels were similar. Our data suggest that NO may play a role in regulating venous tone under baseline conditions and that the role of NO in regulation of vasomotor tone becomes more significant in the presence of nonspecific elevation of vasomotor tone in both arteries and veins. We speculate that endogenous NO production may be one mechanism by which pulmonary and systemic vessels counter the effects of vasoconstrictive agents.
我们已经确定了内源性一氧化氮(NO)在调节绵羊肺内血管和肠系膜血管的血管舒缩张力方面的作用,这些血管处于静息张力和血管舒缩张力升高的状态。从20只绵羊身上分离出直径为2-3毫米的第三代肺内血管环和肠系膜血管环。通过NO合酶的竞争性抑制剂NG-硝基-L-精氨酸甲酯(L-NAME)诱导的张力变化来评估血管中NO的产生。在处于静息张力的血管中,10^(-4)至10^(-3) M的L-NAME仅在静脉中诱导张力显著增加,而在动脉中则没有。当用去氧肾上腺素或血栓素A2类似物U 46,619使张力升高时,现在10^(-4) M的L-NAME在动脉中诱导张力显著增加,10^(-5) M的L-NAME在静脉中诱导张力显著增加。L-NAME在静脉中诱导的张力增加大于在动脉中,并且在张力升高时比在静息张力下更大。肺血管和肠系膜血管的反应相似。我们的数据表明,NO可能在基线条件下调节静脉张力中发挥作用,并且在动脉和静脉血管舒缩张力非特异性升高的情况下,NO在调节血管舒缩张力中的作用变得更加显著。我们推测内源性NO的产生可能是肺血管和全身血管对抗血管收缩剂作用的一种机制。