Mazzocchi G, Rebuffat P, Gottardo G, Nussdorfer G G
Department of Anatomy, University of Padua, Italy.
Life Sci. 1996;58(10):839-44. doi: 10.1016/0024-3205(96)00017-3.
Adrenomedullin (ADM) and calcitonin gene-related peptide (CGRP) did not affect either basal or ACTH-stimulated secretion of a1dosterone and corticosterone by dispersed rat capsular and inner adrenocortical cells, respectively. However, both peptides strongly depressed angiotensin-II (ANG- II)-stimulated a1dosterone production by capsular cells, the minimal effective concentration was 10(-7) M. The inhibitory effect of both ADM and CGRP was reversed by CGRP8-37, a specific CGRP1 receptor antagonist; a complete reversal was obtained with a CGRP8-37 concentration of 10(-6) M. Our findings indicate that ADM and CGRP specifically interfere with the intracellular mechanisms transducing the secretagogue signal of ANG-II, and suggest that the ADM effect is mediated by CGRP receptors
肾上腺髓质素（ADM）和降钙素基因相关肽（CGRP）分别对分散的大鼠被膜和肾上腺皮质内层细胞基础状态下或促肾上腺皮质激素刺激下的醛固酮和皮质酮分泌均无影响。然而，这两种肽均强烈抑制被膜细胞中血管紧张素II（ANG-II）刺激的醛固酮生成，最小有效浓度为10^(-7)M。ADM和CGRP的抑制作用均可被CGRP8-37（一种特异性CGRP1受体拮抗剂）逆转；当CGRP8-37浓度为10^(-6)M时可完全逆转。我们的研究结果表明，ADM和CGRP特异性干扰转导ANG-II促分泌信号的细胞内机制，并提示ADM的作用是由CGRP受体介导的
