Obesity-associated hypertension. Hyperinsulinemia and renal mechanisms.
Obesity-associated hypertension. Hyperinsulinemia and renal mechanisms.
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肥胖相关的高血压。
DOI：
10.1161/01.hyp.19.1_suppl.i45
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发表时间：
1992
期刊：
影响因子：
--
通讯作者：
Mizelle,HL
中科院分区：
文献类型：
--
作者：
Hall,JE;Brands,MW;Hildebrandt,DA;Mizelle,HL
高胰岛素血症和胰岛素抵抗被认为与肥胖和高血压有关。支持这一概念的证据主要来自流行病学研究，表明胰岛素抵抗、高胰岛素血症和血压之间存在相关性，以及短期研究，表明胰岛素具有肾脏和心血管作用，如果持续存在，可能会升高血压。然而，胰岛素和高血压之间的因果关系尚未明确。最近的研究表明，慢性高胰岛素血症，类似于肥胖高血压患者中发现的，并没有提高正常犬的血压，即使肾脏排泄能力降低，事先删除肾脏质量。长期胰岛素输注也未能升高高钠摄入犬的血压，并且不会增强血管紧张素II或去甲肾上腺素的长期血压反应。胰岛素抵抗的存在或不存在可能不是决定高胰岛素血症的血压反应的主要因素，因为长期胰岛素输注也未能引起肥胖、胰岛素抵抗犬的高血压。尽管高胰岛素血症会引起短暂的钠潴留，但在犬中未发生足以引起慢性高血压的肾排泄能力持续下降。在大鼠中，胰岛素输注导致血压小幅升高，尽管高血压的几个特征（例如，盐敏感性）不同于在肥胖的人类高血压患者中观察到的那些。在对胰岛素的长期心血管反应方面，人类是否更接近狗或大鼠仍有待确定。然而，患有胰岛素瘤的人的非常高的胰岛素水平不会引起高血压，并且几项研究表明，正常人的血浆胰岛素浓度和血压之间只有微弱的相关性。因此，除了高胰岛素血症本身之外，其他因素可能是肥胖相关高血压的主要组成部分。
Hyperinsulinemia and insulin resistance have been postulated to link obesity and hypertension. Evidence supporting this concept derives mainly from epidemiological studies showing a correlation between insulin resistance, hyperinsulinemia, and blood pressure and from short-term studies suggesting that insulin has renal and cardiovascular actions that, if sustained, could elevate blood pressure. However, a cause-and-effect relation between insulin and hypertension has not been clearly established. Recent studies indicate that chronic hyperinsulinemia, similar to that found in obese hypertensive patients, did not raise blood pressure in normal dogs, even when renal excretory capability was reduced by prior removal of kidney mass. Chronic insulin infusion also failed to elevate blood pressure in dogs maintained on a high sodium intake and did not potentiate the long-term blood pressure responses to angiotensin II or norepinephrine. The presence or absence of insulin resistance may not be a major factor in determining the blood pressure response to hyperinsulinemia since chronic insulin infusion also failed to cause hypertension in obese, insulin-resistant dogs. Although hyperinsulinemia causes transient sodium retention, sustained decreases in renal excretory capability sufficient to cause chronic hypertension did not occur in dogs. In rats, insulin infusion causes small increases in blood pressure, although several characteristics of the hypertension (e.g., salt-sensitivity) differ from those observed in obese human hypertensive patients. Whether humans more closely resemble dogs or rats with respect to their long-term cardiovascular responses to insulin remains to be determined. However, very high insulin levels in humans with insulinoma do not cause hypertension, and several studies suggest that there is only a weak correlation between plasma insulin concentration and blood pressure in normal humans. Therefore, additional factors besides hyperinsulinemia per se may be responsible for a major component of obesity-associated hypertension.