An altered secretion of adrenocortical and adrenomedullary hormones plays a role in the clinical syndromes of primary aldosteronism (PA), Cushing, and pheochromocytoma. Moreover, an altered production of adrenocortical hormones and/or an abnormal release of factors by the adrenal medulla are involved in several other diseases, including high blood pressure, congestive heart failure, liver cirrhosis, nephrotic syndrome, primary reninism, renovascular hypertension, Addison disease, Bartter, Gitelman, and virilization syndromes. Understanding the regulation of adrenal function and the interactions between adrenal cortex and medulla is, therefore, the prerequisite for mechanistic understanding of these disorders. Accumulating evidence indicates that the modulation of adrenal hormone biosynthesis is a process far more complex than originally thought, as it involves several factors, each cooperating with the other. Moreover, the tight vascular and neural interconnections between the adrenal cortex and medulla underlie physiologically relevant autocrine/paracrine interactions involving several peptides. Besides playing a pathophysiological role in common adrenal diseases, these complex mechanisms could intervene also in rare diseases, such as pheochromocytoma concomitant with adrenal Cushing or with PA, and PA co-occurring with Cushing, through mechanisms that remain to be fully understood at the molecular levels. Heterodimerization of G protein-coupled receptors (GPCRs) induced by peptide signaling is a further emerging new modulatory mechanism capable of finely tuning adrenal hormones synthesis and release. In this review we will examine current knowledge on the role of peptides that act via GPCRs in the regulation of adrenal hormone secretion with a particular focus on autocrine-paracrine signals.

中文翻译：

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肾上腺功能的肽能 G 蛋白偶联受体调节：从工作台到床边和背部。

肾上腺皮质激素和肾上腺髓质激素分泌的改变在原发性醛固酮增多症 (PA)、库欣和嗜铬细胞瘤的临床综合征中起作用。此外，肾上腺皮质激素的产生改变和/或肾上腺髓质因子的异常释放与其他几种疾病有关，包括高血压、充血性心力衰竭、肝硬化、肾病综合征、原发性肾病、肾血管性高血压、艾迪生病、Bartter、Gitelman 和男性化综合症。因此，了解肾上腺功能的调节以及肾上腺皮质和髓质之间的相互作用是了解这些疾病的机制的先决条件。越来越多的证据表明，肾上腺激素生物合成的调节过程远比原先想象的复杂，因为它涉及多个因素，每个因素都相互合作。此外，肾上腺皮质和髓质之间紧密的血管和神经相互连接是涉及多种肽的生理相关自分泌/旁分泌相互作用的基础。除了在常见的肾上腺疾病中发挥病理生理作用外，这些复杂的机制还可以干预罕见疾病，例如伴随肾上腺库欣或 PA 的嗜铬细胞瘤，以及 PA 与库欣共同发生的机制，这些机制在分子生物学方面仍有待充分理解水平。肽信号诱导的 G 蛋白偶联受体 (GPCR) 异二聚化是一种进一步出现的新调节机制，能够微调肾上腺激素的合成和释放。