Natriuretic peptides receptors in human aldosterone-secreting adenomas

Riccardo Sarzani, G. Opocher, M. V. Paci, A. S. Belloni, F. Mantero, P. Dessì-Fulgheri, A. Rappelli

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP) inhibit aldosterone secretion in humans both in vitro and in vivo. Unresponsiveness of aldosterone-secreting adenomas (aldosteronomas) to ANP in vitro and in vivo, might be due to reduced expression of the biologically-active natriuretic peptide receptor type A (NPr-A) and/or increased expression of the clearance receptor for natriuretic peptides (NPr-C). Therefore, we have analyzed NPr gene expression and ANP binding sites in human adrenals and aldosteronomas. Using reverse transcription and polymerase chain reaction, we cloned and characterized cDNAs for NPr-A, NPr-C, and the receptor (NPr-B) for the C-type natriuretic peptide (CNP). Total RNA from three normal human adrenals (obtained at surgery from patients with renal cancer) and five aldosteronomas were used for Northern analysis. NPr-A mRNA (~ 4 kb) and NPr-B mRNA (~ 4 kb) were expressed without significant differences in adrenals and in aldosteronomas except in an aldosteronomas that contained only very low amounts of NPr mRNAs. The gene expression of NPr-C was barely detectable both in adrenals and in aldosteronomas. ANP binding sites were analyzed by autoradiography with 125I-labeled ligand in other six aldosteronomas. Only one of the adenomas analyzed showed ANP binding sites with density of granules similar to nonadenomatous glomerulosa, whereas the others had significantly reduced densities. In summary, aldosteronomas express the genes encoding for NPr but mainly NPr-A, similarly to control adrenals. On the contrary, the binding sites for ANP are greatly reduced in most aldosteronomas. A somatic mutation or a post-transcriptional defect that reduces ANP binding sites might be present in some aldosteronomas.

Original languageEnglish
Pages (from-to)514-518
Number of pages5
JournalJournal of Endocrinological Investigation
Volume22
Issue number7
Publication statusPublished - 1999

Fingerprint

Natriuretic Peptides
Peptide Receptors
Aldosterone
Adenoma
Atrial Natriuretic Factor
Binding Sites
Brain Natriuretic Peptide
Messenger RNA
C-Type Natriuretic Peptide
Gene Expression
Kidney Neoplasms
Autoradiography
Reverse Transcription
Complementary DNA
RNA
Ligands

Keywords

  • Adenoma
  • Aldosterone
  • Human adrenal
  • Natriuretic peptide receptors

ASJC Scopus subject areas

  • Endocrinology

Cite this

Sarzani, R., Opocher, G., Paci, M. V., Belloni, A. S., Mantero, F., Dessì-Fulgheri, P., & Rappelli, A. (1999). Natriuretic peptides receptors in human aldosterone-secreting adenomas. Journal of Endocrinological Investigation, 22(7), 514-518.

Natriuretic peptides receptors in human aldosterone-secreting adenomas. / Sarzani, Riccardo; Opocher, G.; Paci, M. V.; Belloni, A. S.; Mantero, F.; Dessì-Fulgheri, P.; Rappelli, A.

In: Journal of Endocrinological Investigation, Vol. 22, No. 7, 1999, p. 514-518.

Research output: Contribution to journalArticle

Sarzani, R, Opocher, G, Paci, MV, Belloni, AS, Mantero, F, Dessì-Fulgheri, P & Rappelli, A 1999, 'Natriuretic peptides receptors in human aldosterone-secreting adenomas', Journal of Endocrinological Investigation, vol. 22, no. 7, pp. 514-518.
Sarzani, Riccardo ; Opocher, G. ; Paci, M. V. ; Belloni, A. S. ; Mantero, F. ; Dessì-Fulgheri, P. ; Rappelli, A. / Natriuretic peptides receptors in human aldosterone-secreting adenomas. In: Journal of Endocrinological Investigation. 1999 ; Vol. 22, No. 7. pp. 514-518.
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AU - Paci, M. V.

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AU - Mantero, F.

AU - Dessì-Fulgheri, P.

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AB - Atrial natriuretic peptide (ANP) and B-type or brain natriuretic peptide (BNP) inhibit aldosterone secretion in humans both in vitro and in vivo. Unresponsiveness of aldosterone-secreting adenomas (aldosteronomas) to ANP in vitro and in vivo, might be due to reduced expression of the biologically-active natriuretic peptide receptor type A (NPr-A) and/or increased expression of the clearance receptor for natriuretic peptides (NPr-C). Therefore, we have analyzed NPr gene expression and ANP binding sites in human adrenals and aldosteronomas. Using reverse transcription and polymerase chain reaction, we cloned and characterized cDNAs for NPr-A, NPr-C, and the receptor (NPr-B) for the C-type natriuretic peptide (CNP). Total RNA from three normal human adrenals (obtained at surgery from patients with renal cancer) and five aldosteronomas were used for Northern analysis. NPr-A mRNA (~ 4 kb) and NPr-B mRNA (~ 4 kb) were expressed without significant differences in adrenals and in aldosteronomas except in an aldosteronomas that contained only very low amounts of NPr mRNAs. The gene expression of NPr-C was barely detectable both in adrenals and in aldosteronomas. ANP binding sites were analyzed by autoradiography with 125I-labeled ligand in other six aldosteronomas. Only one of the adenomas analyzed showed ANP binding sites with density of granules similar to nonadenomatous glomerulosa, whereas the others had significantly reduced densities. In summary, aldosteronomas express the genes encoding for NPr but mainly NPr-A, similarly to control adrenals. On the contrary, the binding sites for ANP are greatly reduced in most aldosteronomas. A somatic mutation or a post-transcriptional defect that reduces ANP binding sites might be present in some aldosteronomas.

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