EFFECT OF CORTICOTROPIN-RELEASING FACTOR ON ATRIAL-NATRIURETIC-PEPTIDE RELEASE FROM THE ISOLATED-PERFUSED RAT-HEART

Citation
C. Haug et al., EFFECT OF CORTICOTROPIN-RELEASING FACTOR ON ATRIAL-NATRIURETIC-PEPTIDE RELEASE FROM THE ISOLATED-PERFUSED RAT-HEART, Arzneimittel-Forschung, 44-1(5), 1994, pp. 579-582
Citations number
36
Categorie Soggetti
Pharmacology & Pharmacy",Chemistry
Journal title
ISSN journal
00044172
Volume
44-1
Issue
5
Year of publication
1994
Pages
579 - 582
Database
ISI
SICI code
0004-4172(1994)44-1:5<579:EOCFOA>2.0.ZU;2-D
Abstract
The effect of corticotropin releasing factor (CRF) on atrial natriuret ic peptide (ANP) release and its possible modulation by indometacin, n orepinephrine, propranolol and nitro-L-arginine (an inhibitor of the e ndothelium-derived relaxing factor (EDRF) release) was investigated, u sing an isolated perfused rat heart preparation. Bolus injection of 5 mu g CRF, dissolved in 100 mu l perfusion buffet, provoked a significa nt (p < 0.01 vs. control) short-time increase of ANP release. Indometa cin (3 x 10(-5) mol/l) inhibited the CRF-stimulated increase of ANP re lease and decreased the basal ANP secretion (p < 0.01 vs. CRF group). Norepinephrine (10(-9) mol/l slightly, but not significantly, decrease d the CRF-stimulated ANP release and did not change the basal ANP outp ut. Propranolol (3 x 10(-6) mol/l) did not alter ANP release. Nitro-L- arginine (3 x 10(-5) mol/l) increased the basal ANP release (p < 0.01 vs. CRF group) and prolonged the CRF-induced rise of the ANP secretion . The present data suggest that prostaglandins are important mediators of basal and CRF-stimulated ANP release and that EDRF might be a phys iological inhibitor of ANP release.