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A kinetic model for sodium transport via a non‐gastric H+(Na+)/K+ ATPase
Author(s) -
Nadal-Quiros Monica,
Nieves-Gonzalez Aniel,
Moore Leon C.,
Marcano Mariano
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.867.1
Subject(s) - sodium , chemistry , atpase , ion transporter , potassium , biophysics , kinetics , enzyme , biochemistry , membrane , biology , physics , organic chemistry , quantum mechanics
Experimental results have suggested that macula densa (MD) cells have a unique way of regulating cellular sodium concentration via an apical H + (Na + )/K + ‐ATPase. We developed a kinetic model to represent the sodium transport via this transporter. The model assumes a 2:2 stoichiometry for both the hydrogen and sodium cycles. Rate constant values for the hydrogen cycle were obtained from a renal H + /K + ‐ATPase model (A.M. Weinstein, Am J Physiol Renal Physiol 274:F856‐F867, 1998) which were, in turn, based on values obtained from a gastric H + /K + ‐ATPase model (P. Brzezinski et al., Biochim. Biophys. Acta 942:215–219, 1988). Rate constants for the sodium cycle are assumed to be equal to those in the hydrogen cycle. Results showed that sodium extrusion is very sensitive to changes in luminal potassium concentration from 0 to 20 mM. In addition, sodium extrusion as a function of internal sodium concentration saturates at ~70 mM. This ATPase pump model is essential in the development of larger scale models of ion transport by the MD cells. Research supported by MBRS‐RISE grant 2R25GM061151‐09 and by NIH‐NIGMS grant SC1GM084744.