(Hypertension. 1996;27:827-832.)
© 1996 American Heart Association, Inc.
Articles |
Regulation of Na+,K+-ATPase 
-Subunit Expression by Mechanical Strain in Aortic Smooth Muscle Cells
From the Department of Pharmacology and Experimental Therapeutics (E.S.-M., X.L., J.E.S.), Louisiana State University Medical Center, and Department of Physiology (L.J.H.), Tulane University School of Medicine, New Orleans, La.
Correspondence to Dr Emel Songu-Mize, Department of Pharmacology, LSU Medical Center, 1901 Perdido St, New Orleans, LA 70112. E-mail emize@lsumc.edu.
Abstract We have previously demonstrated that vascular sodium
pump activity is stimulated in several rat models of hypertension. In
addition, others have reported an upregulation of mRNA for the
Na+,K+-ATPase 
1-subunit
in hypertension. To test the effect of sustained, cyclic,
stretch-relaxation stimuli on the expression of 1-
and 2-subunits of
Na+,K+-ATPase in vascular smooth muscle
cells, we used the Flexercell strain unit to stretch rat aortic smooth
muscle cells for several days on a collagen-coated silicone
elastomer substratum. Six-second cycles of stretch-relaxation
were applied to obtain 10% average surface elongation (22% maximum)
for 4 days. Control cells were not stretched but were grown on a
similar surface. The effect of Gd3+, a blocker of
stretch-activated channels, was also investigated. At the
end of 4 days, protein expression of 1- and
2-subunits was determined by Western blot
analysis. Intensity of the bands for 1- and
2-subunits was quantified with the use of a computerized
image analyzer. In the stretched cells, both the
1- and the 2-subunit protein-band
intensities were significantly increased compared with those of the
nonstretched cells. Treatment with 50 µmol/L Gd3+ during
the application of stretch prevented the upregulation of
2-expression but not that of
1-expression. Sodium pump activity, the functional
counterpart of Na+,K+-ATPase, was
inhibited as a result of stretch; Gd3+ had no effect on
this variable. Our results suggest that in vascular smooth muscle,
stretch may be a signal for the upregulation of both the
1- and 2-isoforms. However, a
differential response of the two isoforms to the blocker of
stretch-activated channels implies involvement of different
mechanisms. This alteration in protein expression is not reflected in
the function of the enzyme.
Key Words: muscle, smooth, vascular • cells, cultured • Na(+)-K(+)-exchanging ATPase • mechanoreceptors
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