Open AccessPenicillin G Induces H+, K+-ATPase via a Nitric Oxide-Dependent Mechanism in the Rat Colonic Crypt
Author(s) -
Vanessa Baratta,
Valentiorz,
María José Barahona,
Teresa Gisinger,
David C. Mulligan,
John P. Geibel
Publication year - 2020
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.33594/000000305
Subject(s) - nitric oxide , crypt , chemistry , penicillin , mechanism (biology) , atpase , pharmacology , microbiology and biotechnology , biochemistry , medicine , biology , enzyme , antibiotics , organic chemistry , philosophy , epistemology
The colonic H + , K + ATPase (HKA2) is a heterodimeric membrane protein that exchanges luminal K + for intracellular H + and is involved in maintaining potassium homeostasis. Under homeostatic conditions, the colonic HKA2 remains inactive, since most of the potassium is absorbed by the small intestine. In diarrheal states, potassium is secreted and compensatory potassium absorption becomes necessary. This study proposes a novel mechanism whereby the addition of penicillin G sodium salt (penG) to colonic crypts stimulates potassium uptake in the presence of intracellular nitric oxide (NO), under sodium-free (0-Na + ) conditions.