Hereditability Defect in Red‐Cell K in Hypertension

Background: Following our description of an hereditability of a decreased erythrocyte K [K]er independent of cell Na, in essential hypertension (EH), a long‐term study of RBC (K i , Na i , H 2 O) content, plasma (Na, K, Cl, ionized Ca ++ ), trans‐tubular K gradient (TTKG), total body K (TBK) and body water distribution by Bio‐Impedance Analysis was carried out in 185 hypertensives (47±19 y, 57 females; BP 167±11/101±7 mm Hg). Results: All cases had low K i (85.3±6 mmol/l vs 96.2±4 mmol/l in normal, p<0.001) despite normal (82%) or mild elevated Na i (7.2±1.3 mmol/l vs 6.2±1.1 mmol/l in normal, p=NS), despite similar urinary Na excretion (107±22 vs 101±35 mmol/l). Patients with lowest K i (78.3±5 mmol/l) had lower urinary K 21±15 mmol/l), TTKG (4.2±0.7) and higher 12‐h urinary volume (≥1.3 ml/min) than those with higher K i (86.5±6mmol/l, p<0.002), urinary K (39±11mmol/l, p 0.004), TTKG (7.2±1.3) but lower 12‐h urinary volume (≤0.85 ml/min). Reversal of this abnormal K i content in hypertensives was associated with decline and better control of BP (82%), fasting plasma glucose and regression of ST‐T alterations related to LVH hypertrophy (71%) or coronary artery disease (61%). Such body K disturbances, recorded at different month periods, unrelated to age, sex, race or dietary K intake in the hypertensives, and present in half (48%) of their normotensive offspring were implying a defective K mechanism in erythrocyte‐progenitor cells. Conclusion: These observations strongly suggest a critical role of RBC in normal body K homeostasis that is disturbed in EH.