AJP - Heart and Circulatory Physiology, Vol 259, Issue 3 982-H986, Copyright © 1990 by American Physiological Society
Possible modulation of release of atrial natriuretic factor by endothelium-derived relaxing factor
C. F. Sanchez-Ferrer, J. C. Burnett Jr, R. R. Lorenz and P. M. Vanhoutte
Department of Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905.
The aim of the present study was to investigate the influence of inhibitors
of endothelium-dependent relaxing factor on the release of atrial
natriuretic factor from isolated rat atria. Electrical stimulation of the
tissue produced a frequency-dependent increase in secretion of atriopeptide
from basal levels. Saponin (0.3 mg/ml for 45 min) augmented the basal
release of the peptide. Methylene blue (10(-5)M), oxyhemoglobin (10(-6)M),
or hydroquinone (10(-5)M), agents that inhibit the effects of
endothelium-derived relaxing factor by different mechanisms, caused an
increase in the basal secretion of atrial natriuretic factor. Blockade of
cyclooxygenase with indomethacin (10(-5)M) did not alter the release of
atriopeptide, suggesting that it is not controlled by endogenous
prostaglandins. These results would be explained if the inhibitors tested
were to interfere with a factor released continuously from either
endocardial cells or endothelial cells of the atrial blood vessels and
having the same nature as endothelium-derived relaxing factor. Such release
may exert a tonic negative modulatory influence on the secretion of atrial
natriuretic factor.
