Open AccessStimulation of constitutive nitric oxide uniquely and compensatorily regulates intestinal epithelial cell brush border membrane Na absorption
Author(s) -
Palaniappan Balasubramanian,
Manoharan Palanikumar,
Arthur Subha,
Singh Soudamani,
Murughiyan Usha,
Sundaram Uma
Publication year - 2019
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14086
Subject(s) - brush border , cotransporter , enterocyte , nitric oxide , stimulation , chemistry , small intestine , apical membrane , microbiology and biotechnology , intestinal villus , cell , intracellular , homeostasis , epithelial polarity , biophysics , in vivo , membrane , medicine , endocrinology , sodium , biochemistry , biology , vesicle , organic chemistry
Abstract In the mammalian small intestine, sodium is primarily absorbed by Na + /H + exchange ( NHE 3) and Na‐glucose cotransport ( SGLT 1) in the brush border membrane ( BBM ) of villus cells. However, how enhanced cellular constitutive nitric oxide ( cNO ) may affect NHE 3 and SGLT 1 remains unclear. Both in vivo in rabbit intestinal villus cells and in vitro IEC ‐18 cells, administration of NO donor, GSNAP , modestly increased cNO . GSNAP stimulated SGLT 1 in villus and IEC ‐18 cells. The mechanism of stimulation was secondary to an increase in the affinity of SGLT 1 for glucose. The change in SGLT 1 was not secondary to altered Na‐extruding capacity of the cell since Na + /K + ‐ ATP ase was decreased by GSNAP treatment. In contrast, GSNAP inhibited NHE 3 activity in villus cell BBM . The mechanism of NHE 3 inhibition was secondary to reduced BBM transporter numbers. These studies demonstrated that the physiological increase in cNO uniquely regulates mammalian small intestinal NHE 3 and SGLT 1 to maintain Na homeostasis.