Atrial natriuretic peptide enhances cortisol secretion from guinea-pig adrenal gland: Evidence for an indirect paracrine mechanism probably involving the local release of medullary catecholamines

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Abstract. Neuropeptides (NP) B and W are hypothalamic peptides involved in the regulation of feeding and neuroendocrine axes. Evidence has been provided that NPB and NPW act on both the central and the peripheral branches of the rat hypothalamic-pituitary-adrenocortical axis, and we carried out in vivo and in vitro studies to gain insight into this topic. Reverse transcription-polymerase chain reaction showed the expression of NPB, NPW and their receptors in both adrenal cortex (zonae glomerulosa and fasciculata-reticularis) and adrenal medulla, where immunocytochemistry also detected the presence of abundant NPB-and NPW-immunoreactivity. The acute subcutaneous administration of NPB (0.5 or 1.5 nmol/100 g) did not alter ACTH plasma concentration, while that of NPW (1.5 nmol/100 g) decreased it. Neither NPB nor NPW affected the blood level of aldosterone, while both peptides (0.5 nmol/100 g) raised that of corticosterone. NPB (10 -6 M) lowered ACTH-stimulated aldosterone secretion, and basal and ACTH-stimulated corticosterone production from adrenal quarters containing both cortical and medullary tissues. NPW (10 -6 M) enhanced basal aldosterone secretion from adrenal quarters, and the effect was suppressed by the ß-adrenoceptor antagonist l-alprenolol (10 -5 M). NPW did not affect corticosterone production. Collectively, our findings allow us to draw the following tentative conclusions: i) ACTHindependent extra-adrenal mechanism(s) are operative in vivo, by which NPB and NPW stimulate adrenal glucocorticoid, but not mineralocorticoid secretion; ii) in vitro the interaction of NPB with adrenal medulla activates unknown mechanism(s) hampering adrenocortical steroidogenic machinery; and iii) NPW stimulates in vitro aldosterone secretion by enhancing the release of medullary catecholamines, which in turn activate ß-adrenoceptors located on zona glomerulosa cells.

Section: Discussionmentioning

confidence: 69%

Effects of neuropeptides B and W on the rat pituitary-adrenocortical axis: In vivo and in vitro studies

Hochol¹,

Tortorella²,

Ricinski³

et al. 2007

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“…However, the functional interrelationships between adrenal cortex and medulla are well established (reviewed in ref. (34). The possibility that NPB and NPW may be included in this group of peptides, and that this effect may concur to the in vivo glucocorticoid secretagogue action of NPB and NPW is currently being explored in our laboratories.…”

Section: Discussionmentioning

confidence: 99%

Expression of neuropeptides B and W and their receptors in endocrine glands of the rat

Hochol¹,

Belloni²,

Ruciński³

et al. 2006

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Abstract. Neuropeptides B and W (NPB and NPW) have been identified as endogenous ligands of the G protein-coupled receptors (GPR) 7 and 8, which in humans are expressed in the hypothalamus and probably involved in the regulation of energy homeostasis and feeding behavior. GPR8 is absent in the rat, where the GPR8-like receptor (GPR8-LR) has been described. Reverse transcription-polymerase chain reaction detected the expression of NPB, NPW, GPR7 and GPR8-LR mRNAs in the hypothalamus, anterior pituitary, thyroid and parathyroid glands, pancreatic islets, adrenal glands, ovary and testis of the rat. Immunocytochemistry demonstrated the presence of NPB and NPW immunoreactivities in these same glands. Radioimmune assay showed that the bolus intraperitoneal injection of 2 nmol/100 g NPB or NPW raised the plasma levels of parathyroid hormone, corticosterone and testosterone. NPB also increased the blood concentration of thyroxine, and NPW that of ACTH and estradiol. Taken together, these findings allow us to suggest that NPB and NPW play a role in the autocrine-paracrine functional regulation of the endocrine system in the rat.

“…As mentioned in the Introduction, NPY is included in that group of regulatory peptides (VIP and PACAP, tachykinins, endothelins, adrenomedullin and atrial natriuretic peptides) (22,(31)(32)(33)(34) which are able to enhance steroid secretion by eliciting the release of catecholamines, that in turn stimulate adrenocortical cells in a paracrine manner. The following evidence indicates that this mechanism may be involved in the mild in vitro glucocorticoid secretagogue action of NPY on guinea pig adrenal slices: i) in keeping with previous findings (19,22,(35)(36)(37), NPY enhanced E and NE release from guinea pig adrenomedullary tissue; and ii) l-alprenolol, a specific ß1-receptor antagonist, completely abolished cortisol response of guinea pig adrenal slices to NPY, without per se altering basal cortisol secretion. The majority of studies point out that such a catecholamine-mediated paracrine mechanism mainly concerns zona glomerulosa and aldosterone secretion (reviewed in ref.…”

Section: Discussionmentioning

confidence: 99%

“…Dispersed guinea pig inner adrenocortical cells, adrenal slices (containing both cortical and medullary tissue) and medullary tissue fragments were obtained as previously described (22). Dispersed cells and tissue fragments (10 4 cells and 5-6 mg of tissue) were put in Krebs-Ringer bicarbonate buffer with 3% glucose and 0.2% BSA and incubated with NPY (10 -7 M) alone and in the presence of ACTH (10 -9 M) or Ang-II (10 -8 M).…”

Section: Animals and Reagentsmentioning

confidence: 99%

Neuropeptide Y and glucocorticoid secretion from guinea pig adrenal gland: An in vivo and in vitro study

Rao

Macchi²,

Tortorella³

et al. 2007

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Abstract. The effects of neuropeptide Y (NPY) on adrenal glucocorticoid secretion are controversial, and we have investigated this issue in guinea pigs, where, like in humans and cows, the main glucocorticoid hormone is cortisol. In vivo experiments showed that prolonged NPY administration markedly lowered cortisol plasma concentration not only in normal guinea pigs, but also in animals whose hypothalamicpituitary-adrenal axis and renin-angiotensin system had been pharmacologically interrupted by the simultaneous administration of dexamethasone and captopril. In vitro experiments ruled out the possibility that in vivo glucocorticoid anti-secretagogue action of NPY can ensue from a direct effect on the adrenal gland. In fact, NPY did not affect cortisol secretion from dispersed guinea pig inner adrenocortical cells. In contrast, NPY raised cortisol production from adrenal slices containing medullary tissue, and this effect was blocked by the ß-adrenoceptor antagonist l-alprenolol. This finding, coupled with the demonstration that NPY enhanced catecholamine release from guinea pig adrenomedullary tissue, strongly suggests that NPY may stimulate glucocorticoid secretion in this species through an indirect mechanism involving catecholamines, that in a paracrine manner promote the secretion of inner adrenocortical cells. In light of these observations, the conclusion is drawn that the in vivo effects of NPY are mediated by mechanism(s) independent of either the suppression of the main adrenal agonists ACTH and angiotensin-II or the direct inhibition of adrenal secretion. The possibility merits an investigation into whether NPY enhances the production of peptides, which, like leptin, inhibit adrenal glucocorticoid secretion acting as circulating hormones.