Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1980 Feb 21;302(8):431-4.
doi: 10.1056/NEJM198002213020803.

Adrenergic modulation of extrarenal potassium disposal

Adrenergic modulation of extrarenal potassium disposal

R M Rosa et al. N Engl J Med. .

Abstract

We studied the role of catecholamines in the regulation of potassium homeostasis in nine healthy subjects given intravenous potassium chloride (0.5 meq per kilogram of body weight) in the presence and absence of propranolol. Potassium infusion elevated serum potassium 0.6 +/- 0.09 meq per liter (mean +/-S.E.M.). Addition of propranolol augmented the rise (0.9 +/- 0.05 meq per liter) and prolonged the elevation in serum potassium without decreasing urinary potassium excretion. In a separate study, the same potassium load was administered with a concomitant infusion of epinephrine in five subjects. Epinephrine markedly blunted the increment in serum potassium (0.1 +/- 0.06 meq per liter) while reducing renal potassium excretion. Plasma aldosterone was not altered by the experimental procedures. Serum insulin fell minimally in the presence of propranolol but was unaffected by epinephrine. beta-Adrenergic blockade impairs and epinephrine enhances extrarenal disposal of an acute potassium load. These findings suggest that in patients with impaired potassium disposal, the risk of hyperkalemia may be increased when sympathetic blockade is induced.

PubMed Disclaimer

Publication types

MeSH terms

LinkOut - more resources