Nonuniform regional sympathetic nerve responses to hyperinsulinemia in rats.
Nonuniform regional sympathetic nerve responses to hyperinsulinemia in rats.
复制标题
大鼠对高胰岛素血症的区域交感神经反应不均匀。
DOI：
10.1152/ajpregu.1993.264.2.r423
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Mark,AL
中科院分区：
文献类型：
--
作者：
Morgan,DA;Balon,TW;Ginsberg,BH;Mark,AL
高血压的胰岛素假说提出，高胰岛素血症会增加交感神经活动（SNA）并升高动脉压。本研究的目的是 1) 确定高胰岛素血症是否会导致 SNA 区域均匀或不均匀增加，2) 检验自发性高血压大鼠 (SHR) 对高胰岛素血症具有夸大交感肾上腺反应的假设。我们测量了α-氯醛糖麻醉的 SHR 和血压正常的 Wistar-Kyoto (WKY) 大鼠在输注两剂胰岛素之前和期间的血浆胰岛素、血糖、平均动脉压以及肾上腺、肾脏和腰椎 SNA，每次 60 分钟，同时保持血糖正常。在 WKY 大鼠中，血浆胰岛素从 27 +/- 5 (SE) 分级增加到 200 +/- 29 microU/ml，使腰椎 SNA 从 100% 增加到 285 +/- 26%，但未能显着增加肾上腺或肾脏 SNA。在 SHR 大鼠中，血浆胰岛素从 27 +/- 4 到 213 +/- 33 microU/ml 的类似增加导致肾上腺（100% 到 174 +/- 16%）和腰椎（100% 到 307 +/- 26%）SNA 显着增加，但肾 SNA 没有显着增加。尽管 SNA 有所增加，但两组大鼠的平均动脉压均没有显着增加。我们得出的结论是：1）高胰岛素正常血糖钳夹导致交感神经活动局部不均匀增加，2）在高胰岛素血症期间，与 WKY 大鼠相比，SHR 中的肾上腺 SNA 显着增加，而腰部 SNA 反应在两种品系中相似，而肾脏 SNA 在两种品系中均没有增加。
The insulin hypothesis of hypertension proposes that hyperinsulinemia increases sympathetic nerve activity (SNA) and raises arterial pressure. The goals of this study were 1) to determine if hyperinsulinemia produces regionally uniform or nonuniform increases in SNA and 2) to test the hypothesis that spontaneously hypertensive rats (SHR) have exaggerated sympathoadrenal responses to hyperinsulinemia. We measured plasma insulin, blood glucose, mean arterial pressure, and adrenal, renal, and lumbar SNA in alpha-chloralose-anesthetized SHR and normotensive Wistar-Kyoto (WKY) rats before and during infusion of two doses of insulin for 60 min each while maintaining euglycemia. In WKY rats, graded increases in plasma insulin from 27 +/- 5 (SE) to 200 +/- 29 microU/ml increased lumbar SNA from 100% to 285 +/- 26% but failed to significantly increase adrenal or renal SNA. In SHR rats, similar increases in plasma insulin from 27 +/- 4 to 213 +/- 33 microU/ml caused significant increases in adrenal (100% to 174 +/- 16%) and lumbar (100% to 307 +/- 26%) SNA but not in renal SNA. Despite increases in SNA, mean arterial pressure did not increase significantly in either group of rats. We conclude that 1) hyperinsulinemic euglycemic clamp produces regionally nonuniform increases in sympathetic nerve activity, and 2) there is a potentiated increase in adrenal SNA in SHR compared with WKY rats during hyperinsulinemia, whereas lumbar SNA responses were similar in the two strains, and renal SNA did not increase in either strain.