Haug C, Grunt M, Schmid S, Steinbach G, Metzele A, Maier V, Keck F S, Grünert A
Institute of Clinical Chemistry, University of Ulm, Fed. Rep. of Germany.
Arzneimittelforschung. 1994 May;44(5):579-82.
The effect of corticotropin releasing factor (CRF) on atrial natriuretic peptide (ANP) release and its possible modulation by indomethacin, norepinephrine, propranolol and nitro-L-arginine (an inhibitor of the endothelium-derived relaxing factor (EDRF) release) was investigated, using an isolated perfused rat heart preparation. Bolus injection of 5 micrograms CRF, dissolved in 100 microliters perfusion buffer, provoked a significant (p < 0.01 vs. control) short-time increase of ANP release. Indomethacin (3 x 10(-5) mol/l) inhibited the CRF-stimulated increase of ANP release and decreased the basal ANP secretion (p < 0.01 vs. CRF group). Norepinephrine (10(-9) mol/l) slightly, but not significantly, decreased the CRF-stimulated ANP release and did not change the basal ANP output. 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 physiological inhibitor of ANP release.
采用离体灌注大鼠心脏标本,研究促肾上腺皮质激素释放因子(CRF)对心房利钠肽(ANP)释放的影响,以及吲哚美辛、去甲肾上腺素、普萘洛尔和硝基-L-精氨酸(一种内皮源性舒张因子(EDRF)释放抑制剂)对其的可能调节作用。将5微克CRF溶解于100微升灌注缓冲液中进行单次推注,可引起ANP释放显著(与对照组相比,p<0.01)短期增加。吲哚美辛(3×10⁻⁵摩尔/升)抑制CRF刺激的ANP释放增加,并降低基础ANP分泌(与CRF组相比,p<0.01)。去甲肾上腺素(10⁻⁹摩尔/升)轻微但不显著地降低CRF刺激的ANP释放,且不改变基础ANP输出。普萘洛尔(3×10⁻⁶摩尔/升)不改变ANP释放。硝基-L-精氨酸(3×10⁻⁵摩尔/升)增加基础ANP释放(与CRF组相比,p<0.01),并延长CRF诱导的ANP分泌升高。目前的数据表明,前列腺素是基础和CRF刺激的ANP释放的重要介质,且EDRF可能是ANP释放的生理抑制剂。