O'Callaghan C J, Komersova K, Louis W J
Department of Clinical Pharmacology and Therapeutics, University of Melbourne, Victoria, Australia.
Blood Press Suppl. 1996;1:18-22.
Epidemiological evidence has linked essential hypertension with impaired tissue sensitivity to insulin (i.e. insulin resistance) and actions which could contribute to elevated blood pressure include renal sodium and water retention, sympathetic nervous system stimulation and effects on vascular smooth muscle cell growth and cation balance. Although insulin has pressor effects in some animal models, similar changes in human studies have only been demonstrable with supraphysiological insulin concentrations. We have recently measured finger blood pressure during a two stage hyperinsulinaemic euglycaemic clamp that produced insulin concentrations within the 'physiological' range. The plasma insulin concentration increased from 7.0 +/- 0.3 mu U.ml(-1) to 28.9 +/- 0.6 mu U.ml(-)and then to 101 +/-1.7 mu U.ml(-1) during the procedure and was associated with an increase in fingers but not arm systolic blood pressure during both low dose (i.e.+ 9.9 +/- 1.9 mmHg vs + 7.5 +/- 2.7 mmHg with control,p <0.05) and high dose insulin (21.9 +/- 2.3 mmHg vs 14.6 +/- 3.1 mmHg, p <0.01). Thus it appears that 'physiological' concentrations of insulin have pressor effects on finger systolic blood pressure that are not detectable more proximally and it is possible that such changes could contribute to the development of sustained elevations of blood pressure.
流行病学证据表明，原发性高血压与组织对胰岛素的敏感性受损（即胰岛素抵抗）有关，而可能导致血压升高的因素包括肾钠水潴留、交感神经系统刺激以及对血管平滑肌细胞生长和阳离子平衡的影响。虽然胰岛素在一些动物模型中具有升压作用，但在人体研究中，类似的变化只有在超生理浓度的胰岛素情况下才能被证实。我们最近在一个两阶段的高胰岛素正常血糖钳夹过程中测量了手指血压，该过程产生的胰岛素浓度处于“生理”范围内。在这个过程中，血浆胰岛素浓度从7.0±0.3μU/ml升高到28.9±0.6μU/ml，然后再升高到101±1.7μU/ml，并且在低剂量（即+9.9±1.9mmHg对比对照组为+7.5±2.7mmHg，p<0.05）和高剂量胰岛素阶段（21.9±2.3mmHg对比14.6±3.1mmHg，p<0.01），手指收缩压均升高，但手臂收缩压未升高。因此，似乎“生理”浓度的胰岛素对手指收缩压有升压作用，而在更近端部位则无法检测到这种作用，并且这种变化有可能导致血压持续升高。
