Rebuffat P, Malendowicz L K, Meneghelli V, Macchi V, Nussdorfer G G
Department of Anatomy, University of Padua, Italy.
Life Sci. 1998;62(14):1217-22. doi: 10.1016/s0024-3205(98)00051-4.
Pancreatic polypeptide (PP) concentration-dependently raised basal corticosterone and cyclic-AMP production of dispersed rat zona fasciculata/reticularis adrenocortical cells, maximal effective concentration being 10(-7) M. 10(-7) M PP also significantly enhanced submaximally (10[-12]/10[-11] M), but not maximally (10[-9]/10[-8] M) ACTH-stimulated corticosterone and cyclic-AMP release. Corticosterone responses to PP were abolished by the specific protein kinase A (PKA) antagonist H-89 (10[-5] M). The selective ACTH-receptor antagonist corticotropin-inhibiting peptide (10[-6] M) annulled corticosterone response to 10(-9) M ACTH, but not to 10(-7) M PP. Collectively, our present findings indicate that PP stimulates glucocorticoid secretion of rat adrenal glands, acting through specific receptors coupled, like those of ACTH, with the adenylate cyclase/PKA-dependent signaling pathway.
胰多肽（PP）能浓度依赖性地升高大鼠分散的束状带/网状带肾上腺皮质细胞的基础皮质酮水平及环磷酸腺苷（cAMP）生成量，最大有效浓度为10⁻⁷ M。10⁻⁷ M的PP还能显著增强亚最大剂量（10⁻¹²/10⁻¹¹ M）促肾上腺皮质激素（ACTH）刺激的皮质酮和环磷酸腺苷释放，但对最大剂量（10⁻⁹/10⁻⁸ M）ACTH刺激的释放无增强作用。特异性蛋白激酶A（PKA）拮抗剂H-89（10⁻⁵ M）可消除皮质酮对PP的反应。选择性ACTH受体拮抗剂促肾上腺皮质激素抑制肽（10⁻⁶ M）可消除皮质酮对10⁻⁹ M ACTH的反应，但不能消除对10⁻⁷ M PP的反应。总体而言，我们目前的研究结果表明，PP通过与ACTH类似的、与腺苷酸环化酶/PKA依赖性信号通路偶联的特异性受体，刺激大鼠肾上腺糖皮质激素的分泌。
