Erythrocyte ouabain binding and intracellular Na+ in normotensive obese women and obese women receiving medication for hypertension.
People with "primary obesity" may be hypertensive because they have lost their ability to compensate for the effect of low Na+-K+-ATPase levels on blood pressure. In obese patients receiving hypertensive medication (n = 13), but not in normotensive nonmedicated patients (n = 42), diastolic blood pressure was inversely correlated with erythrocyte ouabain binding (P less than 0.02) and directly correlated with intracellular Na+ concentration (P less than 0.01). Moreover, there was a stronger inverse relationship between ouabain binding and intracellular Na+ in patients receiving medication for hypertension (P less than 0.01) than in normotensive patients (P less than 0.05). These data suggest that patients receiving hypertensive medication may be less able to compensate than normotensive patients, (a) for the potential effect of Na+-K+-ATPase levels on intracellular Na+ and (b) for the potential effect of intracellular Na+ concentration on diastolic blood pressure. We propose that obese people with low levels of ouabain binding (primary obesity) may have an increased risk of developing hypertension if their compensatory mechanisms fail.
D000328:Adult; D000959:Antihypertensive Agents / Q000627:therapeutic use; D001794:Blood Pressure; D004912:Erythrocytes / Q000378:metabolism*; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000150:complications / Q000188:drug therapy; D008875:Middle Aged; D009765:Obesity / Q000097:blood* / Q000150:complications; D011955:Receptors, Drug / Q000097:blood*; D012964:Sodium / Q000097:blood*; D000254:Sodium-Potassium-Exchanging ATPase / Q000097:blood
D000959:Antihypertensive Agents; D011955:Receptors, Drug; C028996:cardiac glycoside receptors; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase