Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats
Possible involvement of nitric oxide in the central salt-loading-induced cardiovascular responses in conscious rats
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DOI：
10.1016/s0006-8993(02)03982-3
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发表时间：
2003-02-14
期刊：
影响因子：
2.9
通讯作者：
Kannan, H
中科院分区：
文献类型：
--
作者：
Jin, QH;Kunitake, T;Kannan, H
本研究的目的是阐明一氧化氮（NO）在中央盐负荷诱导的心血管反应中的可能参与。采用活体脑微透析技术，用高渗生理盐水（0.3或0.45 M）直接灌注下丘脑室旁核（PVN）区。测量PVN区NO代谢物的细胞外浓度，同时测量血压和心率。0.45 M生理盐水灌注使大鼠BP HR升高，PVN区NO代谢物水平升高；而灌注0.3 M生理盐水仅提高NO代谢物水平，未引起血压和心率的变化。接下来，我们确定一氧化氮是否参与高渗盐水诱导的心血管反应。n - g -甲基- l-精氨酸（N-G-methyl-L-arginine, L-NMMA）预处理能减弱0.45 M生理盐水直接灌注引起的血压和心率升高，而在PVN区直接输注3- morpholmosyndnon亚胺（SIN-1， NO供体）可引起血压和心率升高。这些结果表明，用高渗盐水局部灌注PVN区域可引起NO的局部释放，这可能通过激活一氧化氮合酶来产生心血管反应。(C) 2002 Elsevier Science B.V.版权所有
The objective of this study was to elucidate the possible involvement of nitric oxide (NO) in the cardiovascular responses induced by central salt loading. Direct perfusion of the hypothalamic paraventricular nucleus (PVN) region with hypertonic saline (0.3 or 0.45 M) was performed in conscious rats by using an in vivo brain microdialysis technique. The extracellular concentration of NO metabolites in the PVN region was measured, as were the blood pressure (BP) and heart rate (HR). Perfusion of 0.45 M saline increased the BP HR, and NO metabolite levels in the PVN region; however, perfusion of 0.3 M saline enhanced only the level of NO metabolites but did not induce changes in the BP and HR. Next, we determined whether the NO was involved in the cardiovascular responses induced by hypertonic saline. Pretreatment with N-G-methyl-L-arginine (L-NMMA), an inhibitor of NO synthase, attenuated the increases in the BP and HR induced by direct perfusion of 0.45 M saline, while direct infusion of 3-morpholmosyndnonimine (SIN-1, a NO donor) in the PVN region induced increases in the BP and HR. These results suggest that local perfusion of the PVN region with hypertonic saline elicits a local release of NO, which may be carried out by activating nitric oxide synthase to produce cardiovascular responses. (C) 2002 Elsevier Science B.V. All rights reserved.