Vokurková Martina, Dobesová Zdena, Pechánová Olga, Kunes Jaroslav, Zicha Josef
Center for Experimental Cardiovascular Research, Institute of Physiology, Academy of Sciences of the Czech Republic, Prague, Czech Republic.
Life Sci. 2003 Aug 15;73(13):1637-44. doi: 10.1016/s0024-3205(03)00486-7.
The aim of our study was to search for abnormalities of sodium and potassium transport in erythrocytes of male Wistar rats subjected to chronic L-NAME treatment (40 mg/kg/day) for 4 weeks either from weaning (4-week-old) or in adulthood (12-week-old). Sodium content, Na(+),K(+)-pump and Na(+),K(+)-cotransport activity, cation leaks as well as membrane cholesterol and phospholipid contents were determined in fresh erythrocytes. Chronic inhibition of NO synthase elicited similar blood pressure rise in both age groups which did not differ in the degree of NO synthase inhibition. No significant ion transport abnormalities were disclosed in erythrocytes of young NO-deficient rats, whereas erythrocyte Na(+) content, outward Na(+),K(+)-cotransport and inward Na(+) leak were significantly reduced in adult hypertensive animals compared to age-matched controls. It should be noted that the erythrocytes of adult control rats were characterized by higher activity of Na(+),K(+)-pump and Na(+),K(+)-cotransport, increased Na(+) and Rb(+) leaks and elevated membrane cholesterol content compared to those of young normotensive controls. Increased Na(+) leak and elevated membrane cholesterol content but reduced membrane phospholipid content were revealed in erythrocytes of adult hypertensive rats when compared to young hypertensive rats. It can be concluded that young and adult Wistar rats did not differ in the extent of NO synthase inhibition and blood pressure rise elicited by chronic L-NAME treatment. Our results exclude the important participation of classical sodium transport abnormalities in the pathogenesis of this NO-deficient form of experimental hypertension.
我们研究的目的是探寻雄性Wistar大鼠红细胞中钠和钾转运的异常情况。这些大鼠从断奶时(4周龄)或成年期(12周龄)开始接受为期4周的慢性L-NAME治疗(40毫克/千克/天)。测定新鲜红细胞中的钠含量、钠钾泵和钠钾协同转运活性、阳离子泄漏以及膜胆固醇和磷脂含量。在两个年龄组中,慢性抑制一氧化氮合酶均引起相似的血压升高,且一氧化氮合酶抑制程度无差异。在年轻的一氧化氮缺乏大鼠的红细胞中未发现明显的离子转运异常,而与年龄匹配的对照组相比,成年高血压动物的红细胞钠含量、外向钠钾协同转运和内向钠泄漏显著降低。应当指出的是,与年轻的正常血压对照组相比,成年对照大鼠的红细胞具有更高的钠钾泵和钠钾协同转运活性、增加的钠和铷泄漏以及升高的膜胆固醇含量。与年轻高血压大鼠相比,成年高血压大鼠的红细胞显示钠泄漏增加、膜胆固醇含量升高但膜磷脂含量降低。可以得出结论,年轻和成年Wistar大鼠在慢性L-NAME治疗引起的一氧化氮合酶抑制程度和血压升高中没有差异。我们的结果排除了经典钠转运异常在这种一氧化氮缺乏型实验性高血压发病机制中的重要作用。