Splanchnic circulation is a critical neural target in angiotensin II salt hypertension in rats
Splanchnic circulation is a critical neural target in angiotensin II salt hypertension in rats
复制标题
DOI：
10.1161/hypertensionaha.107.090696
复制
发表时间：
2007-09-01
期刊：
影响因子：
8.3
通讯作者：
Fink, Gregory D.
中科院分区：
文献类型：
--
作者：
King, Andrew J.;Osborn, John W.;Fink, Gregory D.
慢性血管紧张素II（Ang II）输注，在大鼠喂养高盐，从事交感神经系统，以增加静脉紧张。内脏交感神经系统是静脉张力的最重要的调节器，表明内脏交感神经系统活动可能在Ang II盐高血压中增加。我们假设腹腔神经节切除术（CGx），选择性地破坏交感神经支配内脏循环，将减弱动脉压（AP），血管紧张素II盐高血压和静脉张力增加。大鼠喂养2%或0.4%NaCl的仪器，以允许AP的无线电遥测测量的同时，手术CGx或假手术。Ang II通过微型泵（150 ng/kg/min）递送14天。CGx降低AP独立的盐饮食控制期间。CGx显着减弱血管紧张素II高血压大鼠在2%NaCl，但在大鼠喂养0.4%NaCl的影响不大。为了测试CGx通过肾脏去神经支配发挥其作用的可能性，对大鼠进行相同的方案，但接受选择性双侧肾脏去神经支配。去肾神经支配降低AP在控制，但没有保护作用的血管紧张素II高血压，实际上往往会加剧升压反应。最后，单独的大鼠组进行CGx或假手术，并允许重复测量平均循环充盈压，静脉张力的指数。除了减弱血管紧张素II盐高血压，CGx完全防止血管紧张素II盐诱导的平均循环充盈压的增加，并大大减弱对急性神经节阻滞的降压反应。我们的结论是，在高盐的存在下，血管紧张素II激活内脏交感神经系统，增加veneplasm张力和AP。
Chronic angiotensin II (Ang II) infusion, in rats fed high salt, engages the sympathetic nervous system to increase venomotor tone. The splanchnic sympathetic nervous system is the most important regulator of venous tone, indicating that splanchnic sympathetic nervous system activity may be increased in Ang II salt hypertension. We hypothesized that celiac ganglionectomy (CGx), to selectively disrupt sympathetic innervation to the splanchnic circulation, would attenuate arterial pressure (AP), and venous tone increases in Ang II salt hypertension. Rats fed 2% or 0.4% NaCl were instrumented to allow AP measurement by radiotelemetry at the same time as surgical CGx or sham operation. Ang II was delivered by minipump (150 ng/kg per minute) for 14 days. CGx reduced AP independent of salt diet during control. CGx markedly attenuated Ang II hypertension in rats on 2% NaCl but had little effect in rats fed 0.4% NaCl. To test the possibility that CGx exerted its effects via renal denervation, rats were subjected to the same protocol but received selective bilateral renal denervation. Renal denervation decreased AP during control but had no protective effect on Ang II hypertension and actually tended to exacerbate the pressor response. Finally, separate groups of rats underwent CGx or sham operation and were instrumented to allow repeated measures of mean circulatory filling pressure, an index of venous tone. In addition to attenuating Ang II salt hypertension, CGx completely prevented Ang II salt-induced increases in mean circulatory filling pressure and substantially attenuated depressor responses to acute ganglion blockade. We conclude that, in the presence of high salt, Ang II activates the splanchnic sympathetic nervous system to increase venomotor tone and AP.