Hrnciarová M, Hrnciar J, Jakubíková K
Interná klinika A, nemocnica F.D. Roosevelta, Banská Bystrica.
Vnitr Lek. 1995 Feb;41(2):111-6.
The hypothesis of insulin resistance in the pathogenesis of arterial hypertension as part of the hormonal metabolic X syndrome and our 5H syndrome resp. (association of hyperinzulinism with hyperglycaemia-NIDDM-hyperlipoproteinaemia, hypertension and a hyperandrogenic state in women) is based on sympathomimetic, sodium retention and trophic effects of insulin. In the submitted paper the authors review opinions supporting and refuting the validity of this hypothesis. Based on the results of different studies in recent years another genetic predisposition comes also to the foreground, i.e. reduced vascularization of the skeletal muscles which on the background of insulin resistance leads to enhanced development of hypertension with subsequent hypertrophy of the vascular wall and left ventricle and to the development of arteriosclerosis. From the clinical aspect this stimulating pathogenetic concept within the framework of the hormonal and metabolic X syndrome and 5H syndrome makes it possible to use a more adequate approach to prevention and treatment not only of arterial hypertension but also of associated phenomena which enhance the risk of cardiovascular morbidity and mortality in the population. The authors summarize factors which during non-pharmacological treatment promote insulin resistance and those which improve it. When drugs are selected for pharmacological treatment, priority is given to those which improve the insulin sensitivity index (ACE-inhibitors, alpha blockers) or are at least neutral in this respect (Ca antagonists, beta blockers with ISA and cardioselective). The drugs must not enhance associated hyperlipoproteinaemia, hypercoagulability, hyperviscosity, hyperuricaemia) and they should exert a positive effect on the regression of hypertrophic vascular walls and the left ventricle.
作为激素代谢X综合征及我们的5H综合征（女性高胰岛素血症与高血糖 - 非胰岛素依赖型糖尿病 - 高脂蛋白血症、高血压及高雄激素状态的关联）一部分的胰岛素抵抗在动脉高血压发病机制中的假说，基于胰岛素的拟交感神经作用、钠潴留作用及营养作用。在提交的论文中，作者回顾了支持和反驳该假说有效性的观点。基于近年来不同研究的结果，另一种遗传易感性也凸显出来，即骨骼肌血管化减少，在胰岛素抵抗背景下，这会导致高血压的进一步发展，随后血管壁和左心室肥厚以及动脉硬化的发生。从临床角度来看，在激素和代谢X综合征及5H综合征框架内的这一刺激性发病概念，使得不仅对动脉高血压，而且对增加人群心血管发病和死亡风险的相关现象，有可能采用更适当的预防和治疗方法。作者总结了非药物治疗期间促进胰岛素抵抗的因素以及改善胰岛素抵抗的因素。在选择药物进行药物治疗时，优先选择那些能改善胰岛素敏感性指数的药物（血管紧张素转换酶抑制剂、α受体阻滞剂），或者至少在这方面呈中性的药物（钙拮抗剂、具有内在拟交感活性和心脏选择性的β受体阻滞剂）。这些药物不得加重相关的高脂蛋白血症、高凝性、高黏滞性、高尿酸血症，并且它们应对肥厚的血管壁和左心室的消退产生积极作用。
