Endothelin-3 is efficiently extracted by and induces potent
vasoconstriction in human splanchnic and renal vascular beds.
Weitzberg, Eddie, Anette Hems[acute]en, Jan M. Lundberg, and Gunvor
Ahlborg.
Department of Anaesthesiology and Intensive Care, Karolinska
Hospital, Department of Physiology and Pharmacology, Karolinska
Institute, and Department of Clinical Physiology, Huddinge Hospital,
Stockholm, Sweden
APStracts 2:0287A, 1995.
To investigate splanchnic and renal vascular effects and elimination
of endothelin-3 (ET-3), ET-3 (10 pmol kg-1 min-1 for 20 min) was
given intravenously to six healthy male volunteers. Arterial plasma
ET-3-like immunoreactivity (ET-3-Li) increased 10-fold to 111 +/- 31
pmol.l-1 (p<0.01). The initial half-life of plasma ET-3-Li
determined in three subjects was 1.7 +/- 0.2 min. The fractional
extraction of ET-3-Li was 68 +/- 7% in the splanchnic and 63 +/- 4%
in the renal vascular beds. Mean arterial blood pressure fell from 86
+/- 4 mmHg to 94 +/- 4 mmHg (10%) (p<0.05). Splanchnic and renal
blood flows fell by 43 +/- 3% (p<0.05) and 29 +/- 4%
(p<0.05), respectively, during the infusion. Splanchnic and
renal vascular resistances rose by 92 +/- 22% (p<0.05) and 58
+/- 7% (p<0.05). In conclusion ET-3 infusion in humans induces
splanchnic and renal vasoconstriction of similar magnitude as
previously shown during ET-1 infusion, presumably by ETB receptor
activation. Plasma ET-3 is efficiently extracted in the splanchnic
and renal vascular regions.
Received 8 February 1995; accepted in final form 5 June 1995.
APS Manuscript Number A147-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.