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The Influence of Erythropoietin on the Vascular Responses of Rat Resistance Arteries
Author(s) -
Wu Xiao Chun,
Richards Nicholas T.,
Johns Edward J.
Publication year - 1999
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.1999.01910.x
Subject(s) - mesenteric arteries , endocrinology , medicine , vasoconstriction , vasodilation , bradykinin , erythropoietin , chemistry , sodium nitroprusside , blood vessel , agonist , artery , receptor , nitric oxide
SUMMARY This study examined the effect of erythropoietin (EPO) on resting tension and on the responses of rat mesenteric and renal arcuate arteries in vitro to a number of agonists as a possible cause of its blood pressure elevating properties when used therapeutically. Noradrenaline and potassium chloride induced concentration‐dependent vasoconstrictions in both vessel types but the basal tension, maximum tension, and the ‐log concentration producing half‐maximal response (pEC 50 ) were altered in the presence of 0·1 or 20 U ml −1 EPO. The thromboxane A 2 receptor agonist U46619 induced a constriction of the renal arcuate arteries which was enhanced by EPO at 20 U ml −1 , from 1·68 ± 0·34 to 2·64 ± 0·39 mN mm −1 ( P < 0·01), but which was unchanged by N G ‐nitro‐L‐arginine methyl ester (10 −4 m). Serotonin (10 −9 ‐10 −5 M) caused a concentration‐related vasoconstriction in renal arcuate arteries which was shifted to the right in the time control study ( P < 0·001) but this was abolished by both 0·1 and 20 U ml −1 of EPO. Acetylcholine induced a relaxation of precontracted mesenteric arteries, by 95·4 ± 1·64% with an EC 50 of 7·08 ± 0·08 M which was reduced ( P < 0·001) by 20 U ml −1 EPO to 81·7 ± 3·56% and 6·10 ± 0·11 M, respectively. The sodium nitroprusside‐induced relaxations were unaffected by EPO. The acetylcholine‐mediated relaxations in renal arcuate arteries were unchanged by EPO. Bradykinin‐induced relaxations in mesenteric and renal arcuate arteries were unaffected by both EPO concentrations. Together these data showed that EPO over a large concentration range had only minor effects on basal tension and the vascular responsiveness of both mesenteric and renal arcuate arteries. The mechanism whereby EPO causes a chronic elevation in blood pressure is unlikely to be due to acute interactions with agonist‐mediated responses.