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Hemodynamic Effects of Endothelin-1 and Big Endothelin-1 in Chronic Hemodialysis Patients

ASTRID OTTOSSON-SEEBERGER^*, GUNVOR AHLBORG, ANETTE HEMSÉN, JAN M. LUNDBERG and ANDERS ALVESTRAND^*

^* Division of Renal Medicine, Department of Clinical Science, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden.
Division of Clinical Physiology, Department of Medical Laboratory Sciences & Technology, Huddinge University Hospital, Karolinska Institute, Huddinge, Sweden.
Division of Pharmacology, Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.

Correspondence to Dr. Astrid Ottosson-Seeberger, Division of Renal Medicine K 56, Huddinge Hospital, S-141 86 Huddinge, Sweden. Phone: 46 8 585 87 616; Fax: 46 8 711 47 42; E-mail: astrid.ottosson-seeberger{at}renalmed.hs.sll.se

Abstract. Increased plasma concentrations of endothelin-1 (ET-1) and big endothelin-1 (big ET-1) have been reported in patients with end-stage renal failure (ESRD). In the present study, which included hemodialysis (HD) patients with (n = 21) and without (n = 32) ischemic heart disease, the putative association between plasma levels of ET-1 and big ET-1 and ischemic heart disease and the influence of the dialysis procedure on ET concentrations was investigated. This study also examined in an additional five HD patients without cardiac disease whether intravenously infused ET-1 and big ET-1 (0.2, 1, and 4 pmol/kg per min, each dose for 20 min) preserve their vasoactive potency and whether exogenous big ET-1, which in healthy humans is converted in the kidney, is still converted to ET-1 in ESRD. HD patients with ischemic heart disease demonstrated higher plasma levels of ET-1 and big ET-1 than HD patients without this disorder, and HD reduced plasma ET-1 and big ET-1 concentrations. In HD patients, the big ET-1 infusion, resulting in a 1.5-fold increase in plasma ET-1, caused a more marked and prolonged rise in mean arterial BP than ET-1 (20% versus 13%, P = 0.0001) and a slightly smaller but more prolonged decrease in estimated splanchnic blood flow than ET-1 (37% versus 44%, P = 0.02). Furthermore, big ET-1 lowered heart rate by 9% (P = 0.01) but ET-1 did not. Plasma half-lives of ET-1 and big ET-1 were longer in HD patients than in healthy humans. Thus, ET-1 and big ET-1 preserve their vasoactive potency, and circulating big ET-1 is still converted to active ET-1 in ESRD. Consequently, the increased plasma levels of ET-1 and big ET-1 noted in HD patients, especially in patients with ischemic heart disease, might play a role in the development of uremic cardiovascular complications.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673