Nitric oxide opposes myogenic pressure responses predominantly in large arterioles in vivo
Nitric oxide opposes myogenic pressure responses predominantly in large arterioles in vivo
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DOI：
10.1161/01.hyp.31.3.787
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发表时间：
1998-03-01
期刊：
影响因子：
8.3
通讯作者：
Pohl, U
中科院分区：
文献类型：
--
作者：
de Wit, C;Jahrbeck, B;Pohl, U
肌源性血管收缩可能会放大循环血管收缩剂的作用。在提睾小动脉中，研究了生肌成分对静脉输注去甲肾上腺素 (NE) 或血管紧张素 II (Ang II) 收缩的贡献。其次，研究了内皮源性一氧化氮（NO）在控制这些肌源性收缩中的作用及其在阻力血管床中的作用部位。在 30 只麻醉（戊巴比妥）仓鼠中，准备提睾肌用于活体显微镜检查，并将气动血管封堵器放置在主动脉周围以改变动物后躯的血压。静脉输注 NE (0.5 nmol/min) 可使全身血压升高 52+/-2 mm Hg。同时，在小动脉（SA；最大内径，36 至 65 μm）中观察到高达 33+/-6% 的收缩。局部肾上腺素能阻断不会显着改变收缩，但当提睾小动脉的压力升高被腹主动脉部分闭塞阻断时，收缩被消除。然而，大动脉的直径（LA；最大内径，65至127μm）在NE输注后没有显着变化。当通过部分打开主动脉封堵器将局部压力从 60 毫米汞柱逐步增加到 120 毫米汞柱时，在小动脉中观察到类似的反应。然而，用 NO 合酶抑制剂 N-G-硝基-L-精氨酸（L-NNA，30 μmol/L）处理提睾组织后，LA 中出现高达 16+/-3% 的显着压力诱导收缩。而 SA 收缩的幅度保持不变。 L-NNA 还消除了在对照动物中随压力增加而观察到的血液增加。当Ang II 用于升高血压时也得到了类似的结果。我们得出的结论是，SA 的肌源性收缩对提睾小动脉对循环血管收缩剂的整体反应有显着贡献。 NO 有效地对抗 LA 中的肌源性反应，从而防止血管区域的肌源性收缩，而代谢扩张无法完全控制收缩。如果NO对肌源性收缩的这种减弱作用也发生在其他器官中，那么它可能是控制血管收缩剂引起的总外周血管阻力变化的决定性机制。
A myogenic vasoconstriction may amplify the effects of circulating vasoconstrictors. In cremaster arterioles, die contribution of a myogenic component to the constriction on intravenous infusion of norepinephrine (NE) or angiotensin II (Ang II) was studied. Second, the role of endothelium-derived nitric oxide (NO) in the control of these myogenic constrictions and its site of action in the resistance vascular bed was investigated. In 30 anesthetized (pentobarbital) hamsters, the cremaster was prepared for intravital microscopy, and a pneumatic vessel occluder was placed around die aorta to vary blood pressure in the hindquarter of the animal. Intravenous infusion of NE (0.5 nmol/min) increased the systemic blood pressure by 52+/-2 mm Hg. Simultaneously, constrictions of up to 33+/-6% were observed in the small arterioles (SAs; maximal inner diameter, 36 to 65 mu m). The constrictions were not significantly altered by a local adrenergic blockade but were abolished when the pressure elevation in the cremaster arterioles was blocked by partial occlusion of the abdominal aorta. Diameters in large arterioles (LAs; maximal inner diameter, 65 to 127 mu m), however, did not change significantly on NE infusion. Similar responses in the arterioles were observed when die local pressure was increased stepwise from 60 to 120 mm Hg by partial opening of the aortic occluder. However, after treatment of the cremaster tissue with the inhibitor of the NO synthase, N-G-nitro-L-arginine (L-NNA, 30 mu mol/L), a significant pressure-induced constriction of up to 16+/-3% occurred in LAs. whereas the magnitude of the constriction in SAs remained unchanged. L-NNA also abolished the increases in blood now that were observed with increments in pressure in control animals. Similar results were obtained when Ang II was used to increase blood pressure. We conclude that a myogenic constriction of SAs contributes markedly to the overall response of cremaster arterioles to circulating vasoconstrictors. NO effectively opposes the myogenic response in LAs, thus preventing myogenic constrictions in a vascular region where constriction cannot be fully controlled by metabolic dilation. If this attenuating effect of NO on myogenic constriction also takes place in other organs, it might be a decisive mechanism in controlling changes of total peripheral vascular resistance elicited by vasoconstrictors.