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抑制葡萄糖后高胰岛素血症对正常血压或高血压受试者的血压均无影响。

Suppression of post-glucose hyperinsulinaemia does not affect blood pressure in either normotensive or hypertensive subjects.

作者信息

Savage M W, Mohamed-Ali V, Williams G

机构信息

Department of Medicine, University of Liverpool, U.K.

出版信息

Clin Sci (Lond). 1998 Jun;94(6):609-14. doi: 10.1042/cs0940609.

DOI:10.1042/cs0940609
PMID:9854458
Abstract
  1. Hyperinsulinaemia and insulin resistance are thought to be intimately involved in the development of hypertension, but controversy remains as to whether hyperinsulinaemia is a consequence or a cause of hypertension per se, and whether it plays a role in the short-term regulation of blood pressure. 2. We studied six hypertensive patients [blood pressure 161(9)/101(2) mmHg] and seven normotensive control subjects [blood pressure 122(6)/76(4) mmHg], (P < 0.005) using two oral glucose tolerance tests of 3 h duration. In one of these tests the endogenous insulin response was inhibited with subcutaneous octreotide. 3. After placebo, hypertensive patients had slightly but significantly higher blood glucose levels than controls (P < 0.0001), but comparable insulin concentrations (P > 0.5). Plasma noradrenaline levels were consistently lower in the hypertensive group (P < 0.001). Blood pressure did not change in either group during the 3 h after glucose ingestion. 4. Octreotide completely abolished the immediate insulin response to glucose in all subjects (both P < 0.0001) and caused a delayed and significantly increased glycaemic response in both groups (P < 0.0001). There were no significant differences in plasma glucose responses between groups: however, after octreotide, the hypertensive subjects had a greater insulin suppression than the controls (P < 0.02). Octreotide suppressed noradrenaline levels in the normotensive group (P < 0.001); they were also suppressed in the hypertensive group, but just failed to reach significance (P = 0.056). Throughout the study the hypertensive group's noradrenaline levels remained generally lower than those in the control group (P < 0.0001). 5. In this study there were no differences between hypertensive and normotensive subjects in fasting or post-glucose insulin levels, nor any significant change in blood pressure in either group when post-glucose hyperinsulinaemia was suppressed. This argues against insulin playing a direct role in the short-term regulation of blood pressure.
摘要
  1. 高胰岛素血症和胰岛素抵抗被认为与高血压的发生密切相关,但关于高胰岛素血症本身是高血压的结果还是原因,以及它是否在血压的短期调节中起作用,仍存在争议。2. 我们使用两个持续3小时的口服葡萄糖耐量试验,研究了6名高血压患者[血压161(9)/101(2) mmHg]和7名血压正常的对照者[血压122(6)/76(4) mmHg],(P < 0.005)。在其中一个试验中,用皮下注射奥曲肽抑制内源性胰岛素反应。3. 服用安慰剂后,高血压患者的血糖水平略高于但显著高于对照组(P < 0.0001),但胰岛素浓度相当(P > 0.5)。高血压组的血浆去甲肾上腺素水平始终较低(P < 0.001)。在摄入葡萄糖后的3小时内,两组的血压均未变化。4. 奥曲肽完全消除了所有受试者对葡萄糖的即时胰岛素反应(两者P < 0.0001),并导致两组的血糖反应延迟且显著增加(P < 0.0001)。两组之间的血浆葡萄糖反应无显著差异;然而,使用奥曲肽后,高血压受试者的胰岛素抑制程度大于对照组(P < 0.02)。奥曲肽降低了血压正常组的去甲肾上腺素水平(P < 0.001);高血压组的去甲肾上腺素水平也有所降低,但未达到显著水平(P = 0.056)。在整个研究过程中,高血压组的去甲肾上腺素水平总体上仍低于对照组(P < 0.0001)。5. 在本研究中,高血压患者和血压正常的受试者在空腹或葡萄糖后胰岛素水平上没有差异,当葡萄糖后高胰岛素血症被抑制时,两组的血压也没有任何显著变化。这表明胰岛素在血压的短期调节中不发挥直接作用。

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