Adrenal neuropeptides: Regulation and interaction with ACTH and other adrenal regulators

Abstract

It is now well accepted that both the cortex and medulla of the mammalian adrenal gland receive a rich innervation. Many different transmitter substances have been identified in nerves supplying both cortex and medulla and, as well as catecholamines, a wide range of neuropeptides has been found in the adrenal gland. There have been several studies on the affects of age, sodium intake, stress, ACTH, and splanchnic nerve activity on the regulation of adrenal neuropeptide content. There is evidence that the abundance of each of these peptides is actively regulated. Although there have been many studies addressing the individual actions of various neurotransmitters on steroid secretion, adrenal blood flow, and adrenal growth, few have attempted to determine the nature of any interaction between neurotransmitters and the classical adrenal stimulants. There are, however, some significant interactions, particularly in the regulation of zona glomerulosa function. This review necessarily focuses on vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), as these are the most abundant transmitter peptides in the adrenal gland and the majority of studies have investigated their regulation and actions. However, substance P, calcitonin gene-related peptide (CGRP), neurotensin, and the enkephalins are included where appropriate. Finally, it has been suggested that certain neurotransmitters, particularly VIP, may interact with classical hormone receptors in the adrenal, notably the ACTH receptor. This review attempts to evaluate our current state of knowledge in each of these areas.

Physiological Roles of Prolactin in the Adrenocortical Response to Acute Restraint Stress

“…PRL-R mRNA has been detected in both the adrenal cortex and medulla of many species [7,[11][12][13]. Adrenal sensitivity to ACTH is regulated by adrenal innervation (for example, splanchnic nerve stimulation) with the subsequent release of catecholamines and vasoactive neuropeptides that affect adrenal blood flow and hence, increase the presentation of ACTH to the steroidogenic cells of the adrenal cortex and result in an increase of corticosterone release [50][51][52][53][54][55][56][57][58]. Indeed, while accumulated evidence shows the effect of PRL on adrenal innervation remains controversial, the physiological role of PRL, whether circulating or intraadrenal, in this interplay requires further investigation.…”

Mechanisms of adrenal gland growth: signal integration by extracellular signal regulated kinases1/2

“…In mice, zonation of the cortex occurs soon after birth. Although the classical view of a concentric arrangement and a strict separation of the different adrenal zones is oversimplified (Whitworth et al 2003), the adrenal cortex can roughly be divided into three different zones: the outer zona glomerulosa, followed by the zona fasciculata and the zona reticularis which directly surrounds the medulla. In mice, a functional zona reticularis is absent, instead, the so-called X-Zone can be found during certain postnatal developmental stages in mice.…”

Hormonal and Neural Mechanisms Regulating Hormone Steroids Secretion

“…The VIP and neuropeptide Y (NPY) are the most abundant transmitter-peptides in the adrenal gland (Whitworth et al, 2003). These peptides act as neurotransmitters and exert endocrine, paracrine or autocrine effects in numerous cell types, particularly in the adrenals and ovaries.…”