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Enalapril stimulation of Na pump in crude rat brain synaptosomes, and porcine cardiac membranes

, : Enalapril stimulation of Na pump in crude rat brain synaptosomes, and porcine cardiac membranes. Society for Neuroscience Abstracts 26(1-2): Abstract No -730 6

Enalapril maleate (50 muM) produces prompt hyperpolarization (6.8 mV) of isolated cardiac fibers (De Mello et al., J. Card. Fail. 1997, 3:53-61). Although enalapril is marketed as an inhibitor of angiotensin converting enzyme (ACE). hyperpolarization is not produced by other ACE-inhibitors nor by its active metabolite, enalaprilic acid (enalaprilat). Since the hyperpolarization is ouabain-suppressible, the present study was conducted to determine if enalapril stimulates the Na,K-ATPase. Two preparations were studied, including crude rat brain synaptosomes and porcine cardiac ventricle membranes. Na,K-ATPase actvity was detected as the ouabain-inhibited liberation of inorganic Pi from Tris-ATP by means of a highly sensitive chemical assay (Brotherus et al., BBRC 1981, 100:146-154). Na,K-ATPase activity was stimulated 2-fold within the range Na+ = 2.5 - 50 mM. Captopril (50 muM), a related ACE-inhibitor, had no significant stimulatory effect. Affinity for K+ was not altered. These results suggest that enalapril stimulates the Na,K-ATPase by increasing the affinity of the intracellular Na site of Na,K-ATPase within the physiological range for intracellular Na+. As a result of increased Na+ affinity, the available (Na+)i causes greater activation of the Na,K-ATPase, and generates additional pump current and hyperpolarization. Enalapril may be effective as a membrane stabilizer within the central nervous system.


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