Atrial natriuretic hormone. Predictive of the hypokalemic response to thiazide therapy in essential hypertension.

Thiazide diuretics cause hypokalemia in some, but not all patients. Adding a second diuretic with a different mechanism of action greatly increases the chance of inducing hypokalemia. Suggestive causative factors include hyperaldosteronism, acid-base status, and the degree of natriuresis. Atrial natriuretic hormone (ANH), a circulating peptide secreted primarily by the heart in response to changes in intravascular volume, induces a natriuresis by a mechanism distinct from the thiazides. It was previously shown that furosemide and thiazide diuretics can increase plasma ANH levels in some patients, but reduce ANH levels in others. This phenomenon was investigated in 26 patients with uncomplicated essential hypertension to observe the relationships between ANH and changes in serum potassium (K+) in response to chronic hydrochlorothiazide therapy (HCTZ, 50 mg/day for 1 month). Regression analysis demonstrated significant correlations between K+ level after HCTZ and initial ANH (r = 0.68, P less than .001), change in K+ level and initial ANH (r = 0.40, P less than .05), K+ level after HCTZ and change in ANH (r = -0.64, P less than .001), and change in K+ levels and change in ANH levels (r = -0.38, P less than .05). By multivariate analysis, initial ANH level, but not the plasma aldosterone level, was significantly (P less than .05) related to the change in K+ after HCTZ. These results suggest that initial plasma ANH levels are a marker predictive for diuretic-induced hypokalemia.