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首页> 外文期刊>American Journal of Physiology >Role of central catecholaminergic pathways in the actions of endogenous ANG II on sympathetic reflexes.
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Role of central catecholaminergic pathways in the actions of endogenous ANG II on sympathetic reflexes.

机译：中央儿茶酚胺能途径在内源性ANG II对交感神经反射的作用中的作用。

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In the present study, we examined the effect of blockade of the brain stem renin-angiotensin system on renal sympathetic baroreflexes and chemoreflexes in conscious rabbits and examined the role of central catecholaminergic pathways in these responses. Eleven rabbits underwent preliminary surgical instrumentation and pretreatment with central 6-hydroxydopamine (6-OHDA, 500 micrograms/kg) or ascorbic acid 6 wk before the commencement of the experiments. Baroreflex curves were determined under conditions of normoxia and hypoxia (10% O2 + 3% CO2) before and after central administration of either Ringer solution, the ANG II receptor antagonist losartan (10 micrograms), or the angiotensin-converting enzyme inhibitor enalaprilat (500 ng) on separate days. Losartan increased the upper plateau and the range of the mean arterial pressure (MAP)-renal sympathetic nerve activity (RSNA) curve (79 and 78%, respectively) in intact rabbits, whereas this effect was not observed in 6-OHDA-pretreated rabbits. Hypoxia elicited an increase in resting RSNA (111% in intact rabbits and 74% in 6-OHDA-injected rabbits) and elevated the upper plateau of the RSNA-MAP curve in both groups (89% in intact rabbits and 114% in 6-OHDA-injected rabbits). During hypoxia, losartan and enalaprilat increased the RSNA upper plateau in intact rabbits but had no effect in 6-OHDA-pretreated rabbits. No effects on the MAP-heart rate baroreflex curves were observed. Thus the effect of losartan to increase RSNA, particularly during hypoxia and baroreceptor unloading, being abolished by central noradrenergic depletion suggests that the endogenous ANG II which normally causes an inhibition of renal sympathetic motoneurons is dependent on the integrity of central catecholaminergic pathways.
机译：在本研究中，我们检查了脑干肾素-血管紧张素系统的阻断对有意识的兔子的肾交感性压力反射和化学反射的作用，并研究了中央儿茶酚胺能途径在这些反应中的作用。在实验开始前6周，对11只兔子进行了初步的外科手术器械治疗，并用中心6-羟基多巴胺（6-OHDA，500微克/ kg）或抗坏血酸进行了预处理。在正常使用林格溶液，ANG II受体拮抗剂洛沙坦（10微克）或血管紧张素转化酶抑制剂依那普利拉（500）之前和之后，在常氧和低氧（10％O2 + 3％CO2）条件下确定压力反射曲线。 ng）。氯沙坦增加了完整兔的上高原和平均动脉压（MAP）-肾交感神经活动（RSNA）曲线的范围（分别为79％和78％），而在6-OHDA预处理的兔中未观察到这种作用。缺氧引起静息RSNA升高（完整兔为111％，注射6-OHDA的兔为74％），并且两组RSNA-MAP曲线的上平台都升高（完整兔为89％，6--兔为114％） OHDA注射的兔子）。在缺氧期间，氯沙坦和依那普利拉可增加完整兔的RSNA上平台，但对6-OHDA预处理的兔子无作用。没有观察到对MAP心率压力反射曲线的影响。因此，氯沙坦增加RSNA的作用，特别是在低氧和压力感受器卸载过程中，被中枢去甲肾上腺素能耗竭所消除，这表明通常引起肾交感神经元抑制的内源性ANGII取决于中枢儿茶酚胺能途径的完整性。

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