© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Endothelin as a natriuretic hormone: the case for a paracrine action mediated by nitric oxide
Department of Medical Sciences, Division of Biomedical Sciences, Hugh Robson Building, George Square, University of Edinburgh, Edinburgh EH8 9XD, Scotland, UK
* Corresponding author. Tel.: +44-131-651-11-94; fax: +44-131-650-65-27 Yuri.Kotelevtsev@ed.ac.uk
Received 9 February 2001; accepted 19 April 2001
KEYWORDS Blood pressure; Cell communication; Endothelial factors; Renal function
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1 Introduction |
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There is a widely held view that function of the kidney is the key to understanding human essential hypertension. Indeed, all of the currently recognised human monogenic causes of hypertension reflect abnormalities in the genes that determine ion transport in the distal portion of the nephron [1]. It is also recognised that permanent elevation of blood pressure in experimental models of hypertension, and both primary and secondary hypertension in man, requires the shifting of the natriuretic response curve of the kidney towards higher pressures [2]. However, the mechanism underlying pressure-natriuresis, and its resetting in hypertension, remains poorly understood. In this review we have analysed experiments indicating a role for endothelin (ET)-1 as a key natriuretic hormone and propose a new and testable hypothesis for a paracrine action of ET-1 through NO that accommodates the existing experimental findings.
ET-1 is a 21 amino acid peptide, synthesised mainly by endothelial
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2 Physiology of the ET system in the kidney medulla: interaction with NO |
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2.1 Lessons from experimental models
2.2 Functional interactions of ETBR, nNOS and eNOS in renal medulla
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3 Localisation of the ET system and NOS in the kidney |
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4 Hypothesis and its implications |
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5 Opportunities for further experiments |
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