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.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||3 28-3|
|State||Published - 1990|
- guanosine 3',5'-cyclic monophosphate
- isolated rat atrium
ASJC Scopus subject areas