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

Publisher Website
Google Scholar
Abstract
The role of hypokalemia and increased prostaglandin synthesis in the decreased response of blood pressure to i.v. 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 [PGE], treatment with an inhibitor of prostaglandin synthesis corrected the hyperreninemia and restored the pressor response to an angiotensin II to normal but only partially corrected the hypokalemia. In patients with psychogenic vomiting with high urinary PGE, 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 PGE synthesis in the kidney, produces hyperreninemia. An increase in PGE synthesis 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.