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慢性高胰岛素血症与血压。与儿茶酚胺的相互作用?

Chronic hyperinsulinemia and blood pressure. Interaction with catecholamines?

作者信息

Hall J E, Brands M W, Kivlighn S D, Mizelle H L, Hildebrandt D A, Gaillard C A

机构信息

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.

出版信息

Hypertension. 1990 May;15(5):519-27. doi: 10.1161/01.hyp.15.5.519.

Abstract

Although hyperinsulinemia and increased adrenergic activity have been postulated to be important factors in obesity-associated hypertension, a cause and effect relation between insulin, catecholamines, and hypertension has not been established. The aim of this study was to determine whether chronic hyperinsulinemia, comparable with that found in obese hypertensive patients, causes hypertension in normal dogs, increases plasma catecholamines, or potentiates the blood pressure effects of norepinephrine. In six normal dogs, insulin infusion (1.0 milliunits/kg/min) for 7 days, with euglycemia maintained, increased fasting insulin fourfold to sixfold. However, mean arterial pressure did not increase, averaging 99 +/- 2 mm Hg during the control period and 91 +/- 3 mm Hg during the 7 days of insulin infusion. Insulin did not alter plasma norepinephrine or epinephrine, which averaged 171 +/- 27 and 71 +/- 14 pg/ml, respectively, during the control period and 188 +/- 29 and 45 +/- 12 pg/ml during the 7 days of insulin infusion. In six dogs, norepinephrine was infused (0.2 microgram/kg/min) for 7 days to raise plasma norepinephrine to 2,940 +/- 103 pg/ml. Insulin infusion (1.0 milliunits/kg/min) for 7 days during simultaneous infusion of norepinephrine did not further increase mean arterial pressure, which averaged 101 +/- 3 during norepinephrine and 98 +/- 2 mm Hg during insulin plus norepinephrine infusion. Thus, chronic hyperinsulinemia did not increase mean arterial pressure or plasma catecholamines and did not potentiate the blood pressure actions of norepinephrine. These observations provide no evidence that chronic hyperinsulinemia or interactions between insulin and plasma catecholamines cause hypertension in normal dogs.

摘要

尽管高胰岛素血症和肾上腺素能活性增加被认为是肥胖相关性高血压的重要因素,但胰岛素、儿茶酚胺与高血压之间的因果关系尚未确立。本研究的目的是确定与肥胖高血压患者中发现的情况相当的慢性高胰岛素血症是否会导致正常犬类高血压、增加血浆儿茶酚胺,或增强去甲肾上腺素的血压效应。在6只正常犬中,维持血糖正常的情况下,以1.0毫单位/千克/分钟的速度输注胰岛素7天,空腹胰岛素增加了4至6倍。然而,平均动脉压并未升高,对照期平均为99±2毫米汞柱,胰岛素输注7天期间平均为91±3毫米汞柱。胰岛素并未改变血浆去甲肾上腺素或肾上腺素水平,对照期分别平均为171±27和71±14皮克/毫升,胰岛素输注7天期间分别为188±29和45±12皮克/毫升。在6只犬中,以0.2微克/千克/分钟的速度输注去甲肾上腺素7天,使血浆去甲肾上腺素升高至2940±103皮克/毫升。在同时输注去甲肾上腺素期间,以1.0毫单位/千克/分钟的速度输注胰岛素7天并未进一步增加平均动脉压,去甲肾上腺素输注期间平均为101±3,胰岛素加去甲肾上腺素输注期间平均为98±2毫米汞柱。因此,慢性高胰岛素血症并未增加平均动脉压或血浆儿茶酚胺,也未增强去甲肾上腺素的血压作用。这些观察结果没有提供证据表明慢性高胰岛素血症或胰岛素与血浆儿茶酚胺之间的相互作用会导致正常犬类高血压。

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