This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Tunny, T. J. Articles by Stowasser, M. Search for Related Content PubMed PubMed Citation Articles by Tunny, T. J. Articles by Stowasser, M.

(Hypertension. 1995;26:624-627.)
© 1995 American Heart Association, Inc.

Articles

Reduced Renal Extraction of Atrial Natriuretic Peptide in Primary Aldosteronism

Terry J. Tunny; Richard D. Gordon; Shelley A. Klemm; Michael Stowasser

From the Hypertension Unit, Greenslopes Hospital, Brisbane, Queensland, Australia.

Abstract We investigated renal and peripheral forearm extraction of atrial natriuretic peptide in patients with primary aldosteronism to determine whether alterations in extraction may contribute to the elevated levels of circulating atrial natriuretic peptide observed in primary aldosteronism. We obtained simultaneous venous blood samples from the left renal vein and a peripheral vein and from the radial artery in 28 patients with primary aldosteronism and 10 patients with essential hypertension. Renal extraction of atrial natriuretic peptide was significantly (P<.001) reduced (40±2%) in primary aldosteronism compared with essential hypertensive patients (62±3%). Peripheral forearm extraction was also reduced (P<.01) in primary aldosteronism compared with essential hypertensive patients (24±3% versus 38±4%). These findings are consistent with widespread downregulation of atrial natriuretic peptide receptors in primary aldosteronism. Consistent with reports that marked reduction in glomerular filtration rate is required before the renal extraction of atrial natriuretic peptide is reduced, no significant relationship between renal extraction of atrial natriuretic peptide and plasma creatinine was seen in primary aldosteronism or essential hypertension. Although the major regulators of atrial natriuretic peptide secretion in primary aldosteronism are presumably alterations in arterial blood pressure and plasma volume, reduced renal and peripheral extraction of atrial natriuretic peptide in primary aldosteronism may also contribute significantly to the elevated circulating levels observed.

Key Words: hyperaldosteronism • atrial natriuretic factor • human

This article has been cited by other articles:

				C. E. Grim, A. W. Cowley Jr, P. Hamet, D. Gaudet, M. L. Kaldunski, J. M. Kotchen, S. Krishnaswami, Z. Pausova, R. Roman, J. Tremblay, et al. Hyperaldosteronism and Hypertension: Ethnic Differences Hypertension, April 1, 2005; 45(4): 766 - 772. [Abstract] [Full Text] [PDF]

				G. Schreij, P. N. van Es, P. M.H. Schiffers, and P. W. de Leeuw Renal Extraction of Atrial Natriuretic Peptide in Hypertensive Patients With or Without Renal Artery Stenosis Hypertension, June 1, 1996; 27(6): 1254 - 1258. [Abstract] [Full Text]