AJP - Heart and Circulatory Physiology, Vol 261, Issue 6 1895-H1902, Copyright © 1991 by American Physiological Society
Immunoglobulin and renal abnormalities in Dahl genetically hypertensive rat
L. A. Cowen, M. R. Harold, C. M. Chen, R. E. Abbott and D. Schachter
Department of Physiology and Cellular Biophysics, Columbia University College of Physicians and Surgeons, New York, New York 10032.
The Dahl salt-sensitive rat (DS) is a model of genetically determined
arterial hypertension exacerbated by dietary salt. We report two additional
abnormalities of DS rats, which are both genetically determined and
enhanced by salt: 1) immunoglobulin disorders and 2) renal dysfunctions.
These abnormalities precede and are not the result of the arterial
hypertension. In young, prehypertensive DS rats the plasma and tissue
concentrations of immunoglobulin (Ig) G, but not of IgM or IgA, are
decreased compared with those of the salt-resistant strain (DR). A
high-salt diet (8.0% NaCl) decreases the plasma and tissue IgG levels of DS
but not of DR rats. Reduction of IgG in the DS strain results from both
decreased synthesis and increased urinary excretion. Renal dysfunction in
young, prehypertensive DS animals is manifested by increased excretion of
high molecular weight proteins, including albumin, IgG, IgA, and IgM. The
high-salt diet increases the urinary excretion of these proteins within 1-2
days, and the effect is much greater in DS compared with DR rats. The
urinary excretion of IgG is selectively increased relative to
immunoglobulin light chains, IgA and IgM in DS compared with DR animals.
The present studies provide new markers characteristic of the DS phenotype
and pose the issue of possible genetic or functional interrelationships
among the salt-sensitive hypertension, immunoglobulin disorders, and renal
dysfunctions.
