The role of neuropeptides in the regulation of adrenal zona glomerulosa function: effects of substance P, neuropeptide Y, neurotensin, Met-enkephalin, Leu-enkephalin and corticotrophin-releasing hormone on aldosterone secretion in the intact perfused rat adrenal

Abstract

A range of neuropeptides has been identified in the adrenal glands of many mammalian species. In many cases these peptides have been located in nerves supplying the adrenal cortical cells, or within clusters of chromaffin cells within the zona glomerulosa. The function of these neuropeptides has yet to be determined, but from their location within the gland it is clearly possible that they may have a role in the regulation of aldosterone secretion. The effects of Met-enkephalin, Leu-enkephalin, neuropeptide Y, substance P, corticotrophin-releasing hormone (CRH) and neurotensin on aldosterone secretion were investigated using the intact perfused rat adrenal gland in situ. All the peptides tested, except CRH, caused a significant increase in aldosterone secretion over the dose range of 1 pmol to 10nmol, with a maximum response of about a twofold increase in secretion. Met-enkephalin, however, at a dose of 10 nmol caused a 350% increase in aldosterone secretion, a response comparable with that seen in response to angiotensin II in this preparation. These results suggest that, while substance P, neuropeptide Y, neurotensin and Leu-enkephalin all have the capacity to cause modest increases in the rate of steroid secretion by the zona glomerulosa, these neuropeptides probably do not have a major role in the acute regulation of aldosterone secretion, at least under basal conditions. Met-enkephalin, on the other hand, was a more potent stimulus to aldosterone secretion, and thus may have a role in the control of aldosterone secretion.

Modulation of autotransplanted adrenal gland by endothelin‐1: A morphological and biochemical study

“…These data suggest that adrenal-regenerated glandular cells might be, at least in acute experiments, more responsive to ET-1 than to angiotensin 11. ET-1 seems to share some common functional aspects with neuropeptides, which have been clearly evident in the capsule and zona glomerulosa (Hinson et al, 1994). However, according to our present knowledge, ET-1 has not yet been identified in adrenal nerve terminals.…”

Interactions between the neuropeptide Y system and the hypothalamic-pituitary-adrenal axis

“…In addition, results from studies of dogs and rats are inconsistent. It has been shown that only intact NPY can stimulate ACTH and cortisol release in dogs, whereas its C-terminal fragment, NPY (19)(20)(21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)(36), and the NPY analog, NPY (1-36)-OH, are ineffective (12). In contrast, Small et al (18), using different NPY analogs, have obtained results suggesting that the rat hypothalamic NPY receptor, which increased plasma ACTH concentrations, has a fragment activation profile unlike those of Y1-Y4 and Y6 receptors, and appears distinct from the NPY receptor controlling food intake.…”

“…Acute administration of NPY to rats increases the concentrations of circulating aldosterone (24) and enhances the release of aldosterone in adrenals perfused in situ (25) and through isolated specimens of the adrenal capsule and ZG (26). Chronic administration of NPY to rats with damaged HPA axis and renin-angiotensin system (RAS) stimulates ZG to grow and to synthesize steroids (27).…”

“…However, the significance of the stimulatory effect of NPY on the synthesis and release of aldosterone is not very important. This view is based on studies that have demonstrated that the NPY receptor antagonist, Ac-[3-(2,6-dichlorobenzyl)-Tyr 27 ,D-Thr 32 ]NPY(27-36) (PYX-2), does not alter aldosterone release, despite blocking NPY-induced aldosterone secretion (23), and that an NPY-induced increase in aldosterone release is relatively small (29).…”

Effect of acute heat stress on rat adrenal cortex — a morphological and ultrastructural study

“…In these latter zones, due to increased permeability of the capillaries, increased blood flow leaks out into the parenchyma [20]. Alternative or additional explanation takes into consideration the influence of neuropeptide Y (NPY) on the adrenal blood vessels because this peptide causes vasoconstriction [21]. Cold stress cause increases in rat adrenal NPY mRNA [22].…”