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首页> 外文期刊>American Journal of Physiology >Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy.
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Impact of L-NAME on the cardiopulmonary reflex in cardiac hypertrophy.

机译：L-NAME对心脏肥大中心肺反射的影响。

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There is evidence that in cardiac failure, there is defective baroreceptor reflex control of sympathetic nerve activity. Often, cardiac failure is preceded by a state of cardiac hypertrophy in which there may be enhanced performance of the heart. This study investigated whether in two different models of cardiac hypertrophy, there was an increased contribution of nitric oxide (NO) to the low-pressure baroreceptor regulation of renal sympathetic nerve activity (RSNA) and nerve-dependent excretory function. Administration of a volume load, 0.25* body wt/min saline for 30 min, in normal rats decreased RSNA by 40* and increased urine flow by some 9-fold. Following nitro-l-arginine methyl ester (l-NAME) administration, 10 mug.kg(-1).min(-1) for 60 min, which had no effect on blood pressure, heart rate, or RSNA, the volume load-induced renal sympathoinhibitory and excretory responses were markedly enhanced. In cardiac hypertrophy states induced by 2 wk of isoprenaline/caffeine or 1 wk thyroxine administration, the volume challenge failed to suppress RSNA, and there were blunted increases in urine flow in the innervated kidneys, but following l-NAME infusion, the volume load decreased RSNA by 30-40* and increased urine flow by some 20-fold in the innervated kidneys, roughly to the same extent as observed in normal rats. These findings suggest that the blunted renal sympathoinhibition and nerve-dependent diuresis to the volume load in cardiac hypertrophy are related to a heightened production or activity of NO within either the afferent or central arms of the reflex.
机译：有证据表明，在心力衰竭中，交感神经活动的压力感受器反射控制不良。通常，在心脏衰竭之前会出现心脏肥大的状态，在这种状态下心脏的功能可能会增强。这项研究调查了在两种不同的心脏肥大模型中，一氧化氮（NO）是否对低压低压感受器调节肾交感神经活动（RSNA）和神经依赖性排泄功能的贡献增加。在正常大鼠中，在0.25 *体重/分钟的生理盐水中进行30分钟的体积负荷给药，可使RSNA降低40 *，尿液流量增加约9倍。施用硝基-1-精氨酸甲酯（l-NAME）后，持续10 min.kg.kg（-1）.min（-1）60分钟，这对血压，心率或RSNA的体积负荷没有影响诱导的肾交感神经抑制和排泄反应明显增强。在由2周异丙肾上腺素/咖啡因或1周甲状腺素引起的心脏肥大状态中，体积挑战未能抑制RSNA，并且神经支配的肾脏中尿液流量变钝，但是在​​输注l-NAME后，体积负荷降低受支配肾脏中的RSNA增加30-40 *，尿流增加约20倍，与正常大鼠中观察到的程度大致相同。这些发现表明，肾脏肥大的钝性肾交感抑制和神经依赖性利尿作用与反射的传入或中央臂内NO的产生增加或活性增加有关。

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