Hypokalemia,in Bartter's Syndrome and Other Disorders,Produces Resistance to Vasopressors via Prostaglandin Overproduction

Abstract

Summary

The role of hypokalemia and increased synthesis of prostaglandins in the decreased response of blood pressure to intravenous angiotensin II was studied in patients with Bartter's syndrome and in patients with psychogenic vomiting. In patients with Bartter's syndrome with high urinary prostaglandin E, treatment with an inhibitor of prostaglandin synthesis corrected the hyperreninemia and restored the pressor response to angiotensin II to normal but only partially corrected the hypokalemia. In patients with psychogenic vomiting with high urinary prostaglandin E, correction of the hypokalemia corrected the hyperreninemia and restored the pressor response to angiotensin II and to norepinephrine to normal. The findings suggest that hypokalemia, by stimulation of the synthesis of prostaglandin E in the kidney, produces hyperreninemia. An increase in synthesis of prostaglandin E in vascular tissue, stimulated by hypokalemia per se or by angiotensin II (produced by the hyperreninemia) or by both, increases the vascular resistance to angiotensin II and to norepinephrine.