Elsevier

Peptides

Volume 22, Issue 3, March 2001, Pages 429-438
Peptides

Neuropeptide Y and the adrenal gland: a review

https://doi.org/10.1016/S0196-9781(01)00353-9Get rights and content

Abstract

This paper sets out to review several aspects of NPY and adrenal function, starting with the localisation of NPY in the adrenal, then describing the regulation of NPY release and considering whether the adrenal is a significant source of circulating NPY. The review then describes the regulation of adrenal content of peptide, and finally covers the actions of NPY on the adrenal gland, and the receptor subtypes thought to mediate these effects. The regulation and actions of NPY are discussed with reference to both the adrenal cortex and the medulla.

Section snippets

Identification of neuropeptide Y in the adrenal gland

Neuropeptide Y (NPY), originally isolated and characterised in extracts from porcine brain in 1982 [76], was identified in the adrenal gland the following year [1], [52]. Some of the early studies on adrenal NPY looked at species differences in adrenal NPY content, with the mouse and cat found to have higher adrenal NPY content than either the rat or pig [1], [12]. Table 1 compares the adrenal NPY content of various different species and reveals considerable variation, Figure 1, not only

Section B: Actions of NPY on the adrenal

This section will discuss the actions of NPY on the adrenal gland and therefore, will not include the effects of the central administration of NPY on adrenal function which have been discussed elsewhere [55]. A review of the literature reveals that the effects of NPY on the adrenal cortex can vary according to the sex of animals used, the dose of NPY and, in particular, the tissue preparation adopted.

Actions on adrenal growth

In vivo experiments involving long-term exposure either, by repeated ip injection or continuous infusion, have resulted in hypertrophic growth of the zona glomerulosa. Rebuffat et al [69] first demonstrated, using male rats with pharmacologically controlled ACTH and the RAS, a resulting hypertrophic growth in glomerulosa cells following prolonged (seven day) infusion of NPY (20 μg/kg/hr). This chronic treatment was not associated with proliferation of glomerulosa cells, instead, it caused an

Effects on the adrenal medulla

There have been far fewer reports on the actions of NPY on the adrenal medulla than on the cortex, although it does seem to be involved in the inhibition of catecholamine secretion. NPY was found to cause a concentration dependent inhibition of nicotine-stimulated noradrenaline and adrenaline release (IC50 of 1.8 × 10-9M and 1.7 × 10-9M, respectively) from bovine chromaffin cells [21]. Binding studies revealed a single class of saturable binding sites on adrenal medullary membrane preparations

Effects on adrenal blood-flow

Using the in situ perfused rat adrenal preparation NPY caused a dose-dependent inhibition of adrenal blood-flow, probably by vasoconstriction of arterioles entering the tissue capsule. A maximum inhibition was achieved using a single bolus injection of NPY (1 nmol) which resulted in a 30% reduction in perfusion flow-rate. Interestingly, higher doses of NPY (10 nmol) returned flow-rate to basal levels, suggesting a biphasic effect of NPY on the adrenal vasculature [29].

NPY receptors in the adrenal gland

The discovery by quantitative autoradiography of NPY specific binding sites located exclusively in the bovine zona glomerulosa [77] confirms the presence of NPY receptors in the region where they could influence aldosterone secretion. No binding was found in the inner cortical zones or the medulla using this technique. However, studies using membrane fractions from bovine adrenal medullary tissue revealed two populations of NPY receptors [10]. The high affinity receptors had a Kd of 0.26 nM and

Conclusions

Several conclusions may be drawn from the numerous studies on NPY in the adrenal gland:

  • 1.

    NPY is present in both cortex and medulla, in varying quantities, depending on the species and the physiological status of the animal.

  • 2.

    NPY release from the adrenal is increased by splanchnic nerve stimulation, via acetylcholine acting on nicotinic receptors.

  • 3.

    The NPY released from the adrenal probably does not contribute significantly to circulating NPY concentrations.

  • 4.

    The adrenal content of NPY is regulated by

Acknowledgements

We are most grateful to the Wellcome Trust who have provided project grant support for our studies on adrenal neuropeptides.

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    Present address: Department of Endocrinology, Barts and All London, Queen Mary School of Medicine and Dentistry, Suite 12 Dominion House, Bartholomew Close, West Smithfield, London EC1M FBE.

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