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The aim of the present study was to determine first, whether these residues are part of the amiloride binding site, and second, whether they are general determinants of enac block by amiloride and its derivatives. Monogenetic mutations of enac in individuals with inherited forms of hypertension associated with hypokalemia (liddle syndrome) or hypotension associated with hyperkalemia (pseudohypoaldosteronism type 1) underscore the importance of enac in controlling blood pressure as well as blood k + (62, 143). We have investigated the effects of enac αs583, βg525, and γg537 mutations on the kinetics of channel block by amiloride and benzamil
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The role of enac in na + homeostasis and in the control of blood pressure has been demonstrated recently by the identification of mutations in enac β and γ subunits causing hypertension. We now report an investigation of the mechanism of. A missense mutation (g37s) of the human enac β subunit that causes loss of enac function and pha‐1 replaces a glycine that is conserved in the n‐terminus of all members of the enac gene family
