Laboratory of Experimental Hypertension, Institute of Physiology, Czech Academy of Sciences, Prague, Czech Republic.
Physiol Res. 2024 Aug 31;73(Suppl 1):S49-S66. doi: 10.33549/physiolres.935425. Epub 2024 Jul 17.
The study of ontogenetic aspects of water and electrolyte metabolism performed in the Institute of Physiology (Czechoslovak Academy of Sciences) led to the research on the increased susceptibility of immature rats to salt-dependent forms of hypertension since 1966. Hemodynamic studies in developing rats paved the way to the evaluation of hemodynamic mechanisms during the development of genetic hypertension in SHR. A particular attention was focused on altered renal function and kidney damage in both salt and genetic hypertension with a special respect to renin-angiotensin system. Renal damage associated with hypertension progression was in the center of interest of several research groups in Prague. The alterations in ion transport, cell calcium handling and membrane structure as well as their relationship to abnormal lipid metabolism were studied in a close cooperation with laboratories in Munich, Glasgow, Montreal and Paris. The role of NO and oxidative stress in various forms of hypertension was a subject of a joint research with our Slovak colleagues focused mainly on NO-deficient hypertension elicited by chronic L-NAME administration. Finally, we adopted a method enabling us to evaluate the balance of vasoconstrictor and vasodilator mechanisms in BP maintenance. Using this method we demonstrated sympathetic hyperactivity and relative NO deficiency in rats with either salt-dependent or genetic hypertension. At the end of the first decennium of this century we were ready to modify our traditional approach towards modern trends in the research of experimental hypertension. Keywords: Salt-dependent hypertension o Genetic hypertension o Body fluids o Hemodynamics o Ion transport o Cell membrane structure and function o Renal function o Renin-angiotensin systems.
自 1966 年以来,我们在生理学研究所(捷克斯洛伐克科学院)研究水和电解质代谢的个体发生方面,导致了对幼鼠易患盐依赖性高血压形式的研究。发育中的大鼠的血液动力学研究为评估 SHR 遗传高血压发展过程中的血液动力学机制铺平了道路。特别关注了盐和遗传高血压中肾脏功能和肾脏损伤的改变,特别关注了肾素-血管紧张素系统。布拉格的几个研究小组关注与高血压进展相关的肾脏损伤。离子转运、细胞钙处理和膜结构的改变及其与异常脂质代谢的关系,在与慕尼黑、格拉斯哥、蒙特利尔和巴黎的实验室的密切合作中进行了研究。NO 和氧化应激在各种形式的高血压中的作用是与我们的斯洛伐克同事合作进行的研究课题,主要集中在慢性 L-NAME 给药引起的 NO 缺乏性高血压上。最后,我们采用了一种能够评估血管收缩和血管舒张机制在血压维持中平衡的方法。使用这种方法,我们证明了盐依赖性或遗传高血压大鼠的交感神经活性增强和相对 NO 缺乏。在本世纪第一个十年结束时,我们准备修改我们传统的方法,以适应实验性高血压研究的现代趋势。关键词:盐依赖性高血压、遗传高血压、体液、血液动力学、离子转运、细胞膜结构和功能、肾功能、肾素-血管紧张素系统。