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However, as the functions of other channels are critically reliant on membrane voltage, impairment of other transportation procedures may appear. KCNJ10 activity, according to this view, provides a system for indirectly regulating reabsorption of renal tubular sodium, which modulates quantity homeostasis and maintains blood pressure. Indeed, our sufferers, lacking normal KCNJ10 activity, experienced low blood pressure. Moreover, chromosome 1q23.2, where the locus for KCNJ10 resides, has been implicated repeatedly as being linked to blood-pressure variation in different ethnic groups.33-35 In addition, a complete genome scan for the identification of blood-pressure modifiers in hypertensive and normotensive Lyon rat strains showed linkage to the region syntenic to human chromosome 1q23.2.36 Although the current presence of basolateral potassium channels in the renal tubule, including the distal convoluted tubule, is definitely known from electrophysiological studies, the molecular identity of the channels has remained unresolved.37 Our results ought to establish KCNJ10 as a crucial component of basolateral potassium conductance in the distal convoluted tubule.