Abstract
The infusion of the cationic amino l-lysine, l-arginine, or l-ornithine into dogs regularly increases potassium excretion to levels that exceed the filtered load of potassium. Hyperkalemia occurs during the amino acid infusion as a result of displacement of the intracellular potassium by the cationic amino acids. This rise in plasma K is not necessary for the stimulation of K secretion since infusion of the lysine directly into the renal artery produces K secretion without significant change in plasma K. This increased potassium excretion is promptly suppressed by the administration of thiomerin. The effects upon renal K handling in these experiments appear to be the result of facilitation of tubular secretion of K rather than inhibition of reabsorption.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
