Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity.
Nitric oxide modulates arteriolar responses to increased sympathetic nerve activity.
复制标题
一氧化氮调节小动脉反应以增加交感神经活动。
DOI：
10.1152/ajpheart.1996.271.3.h860
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发表时间：
1996
期刊：
影响因子：
--
通讯作者：
Boegehold,MA
中科院分区：
文献类型：
--
作者：
Nase,GP;Boegehold,MA
本研究的目的是确定内源性一氧化氮的作用是否限制了小动脉对交感神经活动增加的反应。采用活体显微镜观察大鼠小肠小动脉（SFA）、一级小动脉（1A）和二级小动脉（2A）对交感神经周围刺激的直径反应。刺激在所有血管类型中诱导频率依赖性收缩，这种收缩被α -肾上腺素能受体拮抗剂酚妥拉明完全消除（10(-6)M）。在SFA和1A中，一氧化氮合酶抑制剂ng -单甲基- l-精氨酸（L-NMMA, 10(-4) M）的存在显著增加了交感神经收缩的程度。在SFA （n = 7）中，3、8和16 Hz的刺激分别诱导了正常过饱和度下11 +/- 1,28 +/- 4,42 +/- 3%的收缩，而L-NMMA存在时则分别为28 +/- 3,46 +/- 5,76 +/- 3%。对于1A (n = 7)，刺激诱导的收缩在正常过浓液下为10 +/- 1,27 +/- 4,37 +/- 3%，而在L-NMMA存在下为24 +/- 2,47 +/- 3,72 +/- 4%。L-NMMA对SFA交感神经收缩的影响（n = 7）被在过液中添加5 × 10(-3) M l -精氨酸完全逆转。这些结果表明，内源性一氧化氮活性可以减轻肠道微血管的交感神经源性收缩。
The purpose of this study was to determine whether arteriolar responses to increased sympathetic nerve activity are limited by the actions of endogenous nitric oxide. Intravital microscopy was used to examine diameter responses of small feed arteries (SFA), first-order arterioles (1A) and second-order arterioles (2A) to perivascular sympathetic nerve stimulation in the superfused rat small intestine. Stimulation induced a frequency-dependent constriction in all vessel types that was completely abolished by the alpha-adrenoceptor antagonist phentolamine (10(-6) M). In SFA and 1A, the magnitude of sympathetic constriction was increased significantly in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine(L-NMMA, 10(-4) M). In SFA (n = 7), stimulation at 3, 8, and 16 Hz induced constrictions of 11 +/- 1, 28 +/- 4, and 42 +/- 3%, respectively, under the normal superfusate vs. 28 +/- 3, 46 +/- 5, and 76 +/- 3% in the presence of L-NMMA. For 1A (n = 7), stimulation induced constrictions of 10 +/- 1, 27 +/- 4, and 37 +/- 3% under the normal superfusate vs. 24 +/- 2, 47 +/- 3, and 72 +/- 4% in the presence of L-NMMA. The effect of L-NMMA on sympathetic constriction in SFA (n = 7) was completely reversed by the additional presence of 5 x 10(-3) M L-arginine in the superfusate. These results suggest that endogenous nitric oxide activity can attenuate sympathetic neurogenic constriction in the intestinal microvasculature.