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Actions of Neuropeptide Y on the Rat Adrenal Cortex¹

Molecular and Cellular Biology Section, Division of Biomedical Sciences, St. Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, London, United Kingdom E1 4NS; and the Clinical Sciences Research Centre, St. Bartholomew’s and the Royal London School of Medicine and Dentistry (S.K.), London, United Kingdom E1 2AT

Address all correspondence and requests for reprints to: Dr. J. P. Hinson, Molecular and Cellular Biology Section, Division of Biomedical Sciences, St. Bartholomew’s and the Royal London School of Medicine and Dentistry, Queen Mary and Westfield College, Mile End Road, London, United Kingdom E1 4NS. E-mail: j.hinson{at}qmw.ac.uk

Although several studies have demonstrated the presence of neuropeptide Y (NPY) in nerves supplying the mammalian adrenal cortex, its function in this tissue remains unclear, with reports of both stimulatory and inhibitory effects on aldosterone secretion apparently depending on the tissue preparation used. In the present study the effects of NPY on rat adrenal capsular tissue were investigated. NPY significantly stimulated aldosterone secretion in a dose-dependent manner, and this effect was abolished by atenolol, a ß₁-adrenergic antagonist. NPY also stimulated the release of catecholamines from intact rat adrenal capsular tissue with the same dose-dependent relationship as the stimulation of aldosterone release. These observations suggest that the actions of NPY may be mediated by the local release of catecholamines from chromaffin cells within adrenal capsular tissue, as we have previously described for vasoactive intestinal peptide.

The second part of this study concerned the NPY receptor subtype mediating the actions of NPY on the adrenal cortex. It was found that peptide YY stimulated aldosterone release with a comparable potency to NPY, whereas pancreatic polypeptide (PP) was without effect. The Y₁ selective NPY analog Leu³¹Pro³⁴NPY had a greater effect on aldosterone release than the Y₂ selective analog NPY_18–36. Studies using the specific Y₁ receptor antagonist BIBP 3226 showed significant attenuation of the aldosterone response to NPY, but no effect on the response to added norepinephrine. Binding studies carried out using [¹²⁵I]NPY revealed the presence of a single population of NPY-binding sites with a K_d of 12.25 nmol/liter and a binding capacity of 623 fmol/mg protein. Competition studies revealed displacement of [¹²⁵I]NPY specific binding by NPY, peptide YY, and Leu³¹Pro³⁴NPY, but not by other peptides. Messenger RNA analysis revealed the presence of messenger RNA coding for both the Y₁ receptor and the Y₄ receptor, but not the other subtypes. Taken together these data suggest that the effects of NPY on the rat adrenal cortex are mediated by the Y₁ receptor subtype.

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