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高胰岛素血症不是皮质醇诱导性高血压的病因。

Hyperinsulinemia is not a cause of cortisol-induced hypertension.

作者信息

Whitworth J A, Williamson P M, Brown M A, Colman P

机构信息

Department of Medicine, St. George Hospital, University of New South Wales, Melbourne, Australia.

出版信息

Am J Hypertens. 1994 Jun;7(6):562-5. doi: 10.1093/ajh/7.6.562.

DOI:10.1093/ajh/7.6.562
PMID:7917157
Abstract

There is much interest in the relationship of hypertension to hyperinsulinemia. Six male volunteers received cortisol, 50 mg orally four times daily, for 5 days. Plasma insulin concentration increased from 11.8 +/- 3.0 mU/L to 16.1 +/- 4.0 mU/L (P = .034). Fasting glucose increased from 4.7 +/- 0.3 to 5.8 +/- 0.1 mmol/L (P = .001). The insulin-to-glucose ratio was unchanged. Octreotide has been reported to lower blood pressure in obese, hyperinsulinemic, hypertensive patients. The hypothesis that cortisol-induced hypertension might be secondary to steroid-induced hyperinsulinemia was examined by determining whether reversal of hyperinsulinemia by octreotide would reverse cortisol-induced hypertension. Five healthy men were given two subcutaneous injections of 0.05 mg of octreotide before and on the fifth day of cortisol administration. Cortisol increased blood pressure, weight, plasma glucose concentration, and white cell count, with decreases in plasma potassium concentration and packed cell volume. Plasma cortisol concentrations were unchanged following octreotide in the control period but decreased after cortisol treatment. Insulin concentrations were reduced profoundly after octreotide, both in the control period (12.5 +/- 3.7 mU/L, falling to 1.1 +/- 0.3 mU/L at 30 min) and on cortisol (22.3 +/- 4.5 to 2.3 +/- 0.5 mU/L at 30 min). Octreotide did not lower pressure before or after cortisol treatment. Thus, octreotide was effective in lowering plasma insulin concentrations but di not lower blood pressure in normal subjects with cortisol-induced hypertension. These data do not support the notion that steroid-induced hyperinsulinemia is responsible for steroid-induced hypertension.

摘要

高血压与高胰岛素血症之间的关系备受关注。六名男性志愿者每天口服4次、每次50毫克皮质醇,持续5天。血浆胰岛素浓度从11.8±3.0毫国际单位/升升至16.1±4.0毫国际单位/升(P = 0.034)。空腹血糖从4.7±0.3毫摩尔/升升至5.8±0.1毫摩尔/升(P = 0.001)。胰岛素与葡萄糖的比值未变。据报道,奥曲肽可降低肥胖、高胰岛素血症、高血压患者的血压。通过确定奥曲肽逆转高胰岛素血症是否会逆转皮质醇诱导的高血压,来检验皮质醇诱导的高血压可能继发于类固醇诱导的高胰岛素血症这一假说。五名健康男性在给予皮质醇前及给药第5天皮下注射两次0.05毫克奥曲肽。皮质醇使血压、体重、血浆葡萄糖浓度和白细胞计数升高,同时血浆钾浓度和红细胞压积降低。在对照期,奥曲肽给药后血浆皮质醇浓度未变,但在皮质醇治疗后降低。在对照期(12.5±3.7毫国际单位/升,30分钟时降至1.1±0.3毫国际单位/升)以及给予皮质醇时(22.3±4.5至30分钟时的2.3±0.5毫国际单位/升),奥曲肽给药后胰岛素浓度均大幅降低。奥曲肽在皮质醇治疗前后均未降低血压。因此,奥曲肽可有效降低血浆胰岛素浓度,但对皮质醇诱导的高血压正常受试者未降低血压。这些数据不支持类固醇诱导的高胰岛素血症导致类固醇诱导的高血压这一观点。

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