抗高血压药改善胰岛素抵抗的药理研究

Pharmacological studies of antihypertensive drugs on improving insulin resistance

综述近 4年来 ,国内抗高血压药物在改善高蔗糖、高盐 -高糖或高果糖喂饲普通大鼠或自发性高血压大鼠胰岛素抵抗 -高血压 (IRH)动物模型和胰岛素抵抗细胞模型的药理效应 ,以及模型的病理、病理生理机制研究进展。结果表明 ,由上述致病因子诱导动物产生高胰岛素血症或胰岛素敏感性降低和胰岛素抵抗是高血压、血糖和脂质代谢紊乱的共同病理生理基础 ,肾素 -血管紧张素 -醛固酮系统、交感神经系统、纤溶 /凝血系统和血管舒缩功能失调 ,是IRH形成的重要因素。IR细胞模型则作为进一步研究IR和药物作用机制。抗高血压药中 ,血管紧张素Ⅱ受体Ⅰ拮抗剂 (AT1RA)、血管紧张素转换酶抑制剂 (A CEIs)、牛磺酸和一些中药方剂等 ,能干预引致IR的病理生理过程中多个不同环节 ,改善了IR ,并产生降压效应。

The progress of pharmacological studies of antihypertensive drugs on improving insulin resistant hypertensive(IRH)animal model induced by feeding of high sugar/high salt and sugar/high fructose diet in usual rats or spontaneously hypertensive rats (SHR),the IR cellular model,and the pathologic and pathophysiological mechanism for above mentioned models were reviewed in 4 years.The results were showed that the common pathophysiological nosogenesis are hyperinsulinemia or insulin sensitivity reduced and IR in the serial animal model with hypertension,metabolic derangement of blood glucose and lipid,and the IR cellular model was acted as the model for mechanism of IR and pharmacologic effects in vitro.The important factors induced IRH are that the dysfunctions of renin angiotensin aldosterone system(RAAS),sympathetic nerve system (SNS)and blood coagulation abnormalities/fibrinolysis,maladjustment of vasodilation or vasoconstriction, have been proved.Several pathophysiological courses induced IR can be interrupted by the antihypertensive drugs,for example of angiotinsinⅡtype Ⅰreceptor antagonists (AT 1RA),converting enzyme inhibitors (ACEIs),taurine and some prescriptions of traditional Chinese medicine,improving insulin resistance and reducing blood pressure.