Studies on erythrocyte acetylcholinesterase in essential hypertension

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.