Walter U
Klin Wochenschr. 1982 Aug 16;60(16):853-7. doi: 10.1007/BF01728352.
There is accumulating evidence that acetylcholinesterase (AChE might be involved in the transport of sodium across biological membranes. Consequently, because in primary hypertension abnormalities in the transport of sodium by red blood cells have been documented. AChE activities were measured in hemoglobin-free red-blood-cell membranes of patients with essential hypertension. In the absence of any effectors, the Michaelis constant of AChE for acetylcholine (Km) was 1.57 . 10(-5) mol/l, both in normotensives and in hypertensives. Sodium inhibited AChE at low substrate concentrations, whereas the enzyme was activated by sodium at moderate and high substrate levels. With increasing sodium, the substrate optimum was displaced toward higher substrate concentration. On the other hand, an inhibition of AChE by excess substrate could be demonstrated. Erythrocyte AChE activity of male patients with essential hypertension was no different from that of the normotensive controls. Therefore, abnormalities in electrolyte transport mechanisms reported in essential hypertension might be independent of AChE activity.
越来越多的证据表明,乙酰胆碱酯酶(AChE)可能参与钠跨生物膜的转运。因此,鉴于原发性高血压患者红细胞钠转运异常已有文献记载,对原发性高血压患者无血红蛋白的红细胞膜中的AChE活性进行了测定。在没有任何效应物的情况下,正常血压者和高血压患者中AChE对乙酰胆碱的米氏常数(Km)均为1.57×10⁻⁵mol/L。在低底物浓度下钠抑制AChE,而在中等和高底物水平时该酶被钠激活。随着钠浓度增加,底物最佳浓度向更高底物浓度偏移。另一方面,可证明过量底物对AChE有抑制作用。原发性高血压男性患者的红细胞AChE活性与正常血压对照者无异。因此,原发性高血压中报道的电解质转运机制异常可能与AChE活性无关。