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Vol. 273, Issue 5, C1739-C1748, November 1997
1 Department of Physiology, Allegheny University of the Health Sciences, Philadelphia, Pennsylvania 19129; and 2 Departmento de Microbiología, Facultad de Medicina, Universidad de Buenos Aires, Paraguay 2155, 1121 Buenos Aires, Argentina
Infection with
human cytomegalovirus (HCMV) causes an enlargement (cytomegaly) of
human fibroblasts (MRC-5). As a first step toward determining whether
solute uptake, mediated in part by Na+/H+
exchange, is responsible for the development of cytomegaly, we studied
the effects of HCMV infection on intracellular pH
(pHi) regulation (nominal
CO2/
concn = 0) by comparing cytomegalic cells with mock-infected cells.
Seventy-two hours after HCMV infection of MRC-5 cells we observed the
following changes relative to mock-infected cells: resting
pHi is 0.1-0.2 pH unit more
alkaline; the intrinsic buffering power of the cytoplasm was reduced by
~40-50%; acid-loading
H+-equivalent fluxes were reduced;
and there were alterations of Na+/H+
exchanger (NHE) properties, including an alkaline shift of the pHi dependence of activity, a
reduction of the apparent affinity for extracellular
Na+, and an increase of the
apparent maximum velocity and a large increase in stimulation by a
hyperosmotic challenge. These results indicate that HCMV infection
exerts a profound effect on functional properties of the NHE, on
acid-loading mechanisms, and on intrinsic cellular buffering power.
These effects are consistent with a role for the NHE in the development
of cytomegaly.
cell volume; acid loading; buffering power; diethyl amiloride
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