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。
