Document Detail


Reduced venous responsiveness to endothelin-1 but not noradrenaline in hypertensive chronic renal failure.
MedLine Citation:
PMID:  11158403     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Endothelin-1 (ET-1), acting mainly through the ET(A) receptor, is a potent endothelium-derived vasoconstrictor peptide. Circulating concentrations of ET-1 are increased in chronic renal failure (CRF) and may influence vascular tone. METHODS: We investigated dorsal hand vein responsiveness to local infusion of ET-1 and noradrenaline in 12 hypertensive and 12 normotensive CRF patients and in 12 age and sex matched control subjects. We also investigated dorsal hand vein responses to the ET(A) receptor antagonist, BQ-123, and the endothelium-independent vasodilator glyceryl trinitrate (GTN), in six patients with CRF. RESULTS: The dose of noradrenaline causing a 50% of maximal vasoconstriction was similar in the hypertensive (32+/-11 pmol/min) and normotensive (26+/-7 pmol/min) CRF patients and control subjects (21+/-6 pmol/min). Vasoconstriction to ET-1 (5 pmol/min) was similar in CRF patients as a whole (AUC 35+/-5%) and controls (32+/-4%; P=0.70). However, venoconstriction was significantly less in hypertensive (23+/-6%) than in normotensive CRF patients (48+/-8%; P=0.01). Overall, venoconstriction to ET-1 correlated inversely with mean arterial blood pressure in the CRF patients (R=-0.43, P=0.04). In addition, basal vein size was smaller, and plasma endothelin concentrations greater, in the hypertensive CRF group. However, infusion of BQ-123 or GTN did not cause venodilatation in these subjects. CONCLUSIONS: These studies are consistent with the hypothesis that elevated plasma ET-1 contributes to vascular tone, and elevated blood pressure, in hypertensive CRF patients, and is associated with vascular receptor downregulation consequent on the increased exposure to ET-1. The reduced vein size in CRF patients appears to be structural rather than functional in nature. Further long-term studies with endothelin antagonists are required to determine the pathophysiological role of ET-1 in the altered structure and function of blood vessels in patients with CRF.
Authors:
M F Hand; W G Haynes; D J Webb
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  16     ISSN:  0931-0509     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2001 Feb 
Date Detail:
Created Date:  2001-02-22     Completed Date:  2001-03-29     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  England    
Other Details:
Languages:  eng     Pagination:  295-301     Citation Subset:  IM    
Affiliation:
Clinical Pharmacology Unit and Research Centre, The University of Edinburgh, Western General Hospital, Edinburgh, UK.
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MeSH Terms
Descriptor/Qualifier:
Dose-Response Relationship, Drug
Endothelin-1 / pharmacology*
Female
Hand / blood supply*
Humans
Hypertension / complications*,  physiopathology*
Kidney Failure, Chronic / complications*,  physiopathology*
Male
Middle Aged
Norepinephrine / pharmacology*
Vasoconstriction
Vasoconstrictor Agents / pharmacology*
Veins / drug effects
Chemical
Reg. No./Substance:
0/Endothelin-1; 0/Vasoconstrictor Agents; 51-41-2/Norepinephrine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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