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首页> 外文期刊>American Journal of Physiology >Baroreceptor reflex regulation in anesthetized transgenic rats with low glia-derived angiotensinogen.
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Baroreceptor reflex regulation in anesthetized transgenic rats with low glia-derived angiotensinogen.

机译：低胶质细胞衍生的血管紧张素原在麻醉的转基因大鼠中的压力感受器反射调节。

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摘要

Endogenous angiotensin (ANG) II and ANG-(1-7) act at the nucleus tractus solitarius (NTS) to differentially modulate neural control of the circulation. The role of these peptides endogenous to NTS on cardiovascular reflex function was investigated in transgenic rats with low brain angiotensinogen (Aogen) due to glial overexpression of an antisense to Aogen (ASrAOGEN) and in Sprague-Dawley (SD) rats. Arterial baroreceptor reflex sensitivity (BRS) for control of heart rate (HR) in response to increases in mean arterial pressure (MAP) was tested before and after bilateral microinjection of the angiotensin type 1 (AT(1)) receptor blocker candesartan or the ANG-(1-7) receptor blocker (d-Ala(7))-ANG-(1-7) into the NTS of urethane-chloralose-anesthetized ASrAOGEN and SD rats. Baseline MAP was higher in ASrAOGEN than in SD rats under anesthesia (P < 0.01). Injection of candesartan or (d-Ala(7))-ANG-(1-7) decreased MAP (P < 0.01) and HR (P < 0.05) in ASrAOGEN, but not SD, rats. The BRS at baseline was similar in ASrAOGEN and SD rats. Candesartan increased BRS by 41% in SD rats (P < 0.01) but was without effect in ASrAOGEN rats. In contrast, the reduction in BRS after (d-Ala(7))-ANG-(1-7) administration was comparable in SD (31%) and ASrAOGEN rats (34%). These findings indicate that the absence of glia-derived Aogen is associated with 1) an increase in MAP under anesthesia mediated via AT(1) and ANG-(1-7) receptors within the NTS, 2) the absence of an endogenous ANG II contribution to tonic inhibition of BRS, and 3) a continued contribution of endogenous ANG-(1-7) to tonic enhancement of BRS.
机译：内源性血管紧张素（ANG）II和ANG-（1-7）作用于孤束核（NTS），以差异地调节循环的神经控制。 NTS内源性这些肽对心血管反射功能的作用已在由于脑胶质对反基因的反义神经胶质过度表达（ASrAOGEN）而导致的低脑血管紧张素原（Aogen）的转基因大鼠中以及在Sprague-Dawley（SD）大鼠中进行了研究。在双向显微注射1型血管紧张素（AT（1））受体阻滞剂坎地沙坦或ANG之前和之后，测试了对平均血压（MAP）升高作出反应以控制心律（HR）的动脉压力感受器反射敏感性（BRS） -（1-7）受体阻滞剂（d-Ala（7））-ANG-（1-7）进入氨基甲酸酯-氯草糖麻醉的ASrAOGEN和SD大鼠的NTS中。麻醉下，ASrAOGEN的基线MAP高于SD大鼠（P <0.01）。注射坎地沙坦或（d-Ala（7））-ANG-（1-7）可降低ASrAOGEN大鼠的MAP（P <0.01）和HR（P <0.05），但不能降低SD大鼠。 ASrAOGEN和SD大鼠的基线BRS相似。坎地沙坦使SD大鼠的BRS升高41％（P <0.01），但对ASrAOGEN大鼠则无影响。相反，施用（d-Ala（7））-ANG-（1-7）后BRS的减少在SD（31％）和ASrAOGEN大鼠（34％）中相当。这些发现表明，不存在胶质细胞源性Aogen与1）NTS内通过AT（1）和ANG-（1-7）受体介导的麻醉下MAP的升高有关; 2）内源性ANG II的缺乏抑制BRS的滋补作用; 3）内源性ANG-（1-7）对BRS的滋补作用的持续贡献。

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