Tubek Sławomir
Faculty of Physical Education and Physiotherapy, Institute of Technology, Opole, and Clinic of Cardiology, Medical Academy, Wrocław, Prószkowska Str. 70, Opole, 45-758, Poland.
Biol Trace Elem Res. 2007 Summer;117(1-3):39-51. doi: 10.1007/BF02698082.
Increased gastrointestinal absorption and urinary excretion of zinc has been confirmed in experimental and clinical studies on primary arterial hypertension as a result from changes of intracellular and extracellular zinc content. In arterial hypertension, the levels of zinc in serum, lymphocyte, and bone decrease while increasing in heart, erythrocytes, kidney, liver, suprarenal glands and spleen. These changes result in the loss of zinc homeostasis that leads to various degrees of deficiency, not entirely compensated by nutritional factors or increased absorption in the gastrointestinal tract. Loss of zinc homeostasis can be both cause and effect of high blood pressure. In the present review, the role of zinc metabolism changes and its mechanisms in arterial hypertension are discussed.
在原发性动脉高血压的实验和临床研究中,由于细胞内和细胞外锌含量的变化,锌的胃肠道吸收和尿排泄增加已得到证实。在动脉高血压中,血清、淋巴细胞和骨骼中的锌水平降低,而心脏、红细胞、肾脏、肝脏、肾上腺和脾脏中的锌水平升高。这些变化导致锌稳态失衡,进而导致不同程度的锌缺乏,营养因素或胃肠道吸收增加并不能完全补偿这种缺乏。锌稳态失衡可能既是高血压的原因,也是其结果。在本综述中,讨论了锌代谢变化及其机制在动脉高血压中的作用。