Parenti P, Villa M, Hanozet G M, Ferrandi M, Ferrari P
Dipartimento di Fisiologia e Biochimica Generali, Università degli Studi di Milano, Italy.
FEBS Lett. 1991 Sep 23;290(1-2):200-4. doi: 10.1016/0014-5793(91)81259-b.
The (Na+,K+)-ATPase activity from the kidney cortex of the Milan hypertensive rat strain (MHS) and the corresponding normotensive control (MNS) was measured both in active solubilized enzyme preparations and in isolated basolateral membrane vesicles. Kinetic analysis of the purified enzyme showed that the Vmax value was significantly higher in MHS rats. The difference between MHS and MNS was not linked to a different number of sodium pumps, but was related to the molecular activity of the enzyme. Using basolateral membrane vesicles, an increased ATP-dependent ouabain-sensitive sodium transport was also demonstrated in MHS rats. These results support the hypothesis that a higher tubular sodium reabsorption may be involved in the pathogenesis of hypertension in this rat strain.
在活性溶解酶制剂和分离的基底外侧膜囊泡中,均对米兰高血压大鼠品系(MHS)及其相应的正常血压对照品系(MNS)肾皮质的(Na +,K +)-ATP酶活性进行了测定。对纯化酶的动力学分析表明,MHS大鼠的Vmax值显著更高。MHS和MNS之间的差异并非与钠泵数量不同有关,而是与酶的分子活性有关。利用基底外侧膜囊泡,还证实了MHS大鼠中ATP依赖性哇巴因敏感的钠转运增加。这些结果支持了以下假设:更高的肾小管钠重吸收可能参与了该大鼠品系高血压的发病机制。