Piera Rebuffat

TL;DR: The 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 C GRP receptors.

TL;DR: Findings suggest that ghrelin acts as an angiostatic molecule and indicate that its activity is comparable to that of a well-known angiOSTatic agent, i.e., vinblastine.

TL;DR: Ghrelin, acting via GHS-Rs exclusively located in the ZG, enhances the growth of human adrenal cortex, through a mechanism involving the activation of the TK-dependent MAPK p42/p44 cascade.

TL;DR: The mechanism underlying the “aldosterone-escape” phenomenon may involve a rise in the intracellular concentration of corticosterone, caused by the enhanced synthesis and activation of 3βHSD and 11βOH.

TL;DR: It is indicated that ETs stimulate the proliferation of rat adrenal ZG cells, acting through ETA receptors coupled with protein kinase C- and tyrosine kinase-dependent signaling pathways, in keeping with the view that in mammals, ZG is the proliferative layer involved in the maintenance of growth of the entire adrenal cortex.