Gans R O, Donker A J
Department of Medicine, Free University Hospital, Amsterdam, The Netherlands.
J Intern Med Suppl. 1991;735:49-64.
Epidemiological evidence suggests that there is a close association between obesity, non-insulin-dependent diabetes (NIDDM) and hypertension. Obesity and NIDDM are the classical insulin-resistant states. Even in the absence of these conditions, essential hypertension is associated with insulin resistance. In view of the acute effects of insulin on renal sodium reabsorption, the sympathetic nervous system, the renin-angiotensin-aldosterone system, the transmembranous cation transport, the cardiovascular reactivity, the atrial natriuretic peptide and the kallikrein-kinin system, hyperinsulinaemia may contribute to the development of hypertension in these diseases. Preliminary evidence suggests that sensitivity to these possible blood-pressure-elevating action(s) of insulin is still present despite the resistance to the glucose-lowering action of the hormone. However, extrapolation of the epidemiological data and results of acute experiments indicate that the impact on blood pressure is rather small. The pathophysiological mechanisms of hypertension in the above-mentioned conditions are also not always consistent with insulin action(s). Moreover, some data suggest that insulin resistance, and not hyperinsulinaemia per se, underlies the blood pressure elevation, while the possibility cannot be excluded that both hypertension and insulin resistance are co-inherited, but unrelated, abnormalities.
流行病学证据表明,肥胖、非胰岛素依赖型糖尿病(NIDDM)与高血压之间存在密切关联。肥胖和NIDDM是典型的胰岛素抵抗状态。即使在没有这些情况时,原发性高血压也与胰岛素抵抗相关。鉴于胰岛素对肾钠重吸收、交感神经系统、肾素 - 血管紧张素 - 醛固酮系统、跨膜阳离子转运、心血管反应性、心房利钠肽和激肽释放酶 - 激肽系统的急性作用,高胰岛素血症可能在这些疾病中导致高血压的发生。初步证据表明,尽管对胰岛素的降糖作用存在抵抗,但对胰岛素这些可能升高血压的作用仍具有敏感性。然而,流行病学数据和急性实验结果的推断表明,其对血压的影响相当小。上述情况下高血压的病理生理机制也并不总是与胰岛素作用一致。此外,一些数据表明,血压升高的基础是胰岛素抵抗而非高胰岛素血症本身,同时也不能排除高血压和胰岛素抵抗是共同遗传但不相关的异常情况的可能性。