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Evidence against potassium as an endothelium‐derived hyperpolarizing factor in rat mesenteric small arteries
Author(s) -
Lacy Peter S,
Pilkington Gemma,
Hanvesakul Rajesh,
Fish Helen J,
Boyle John P,
Thurston Herbert
Publication year - 2000
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1038/sj.bjp.0703076
Subject(s) - potassium , acetylcholine , ouabain , mesenteric arteries , endothelium , chemistry , endocrinology , medicine , myograph , incubation , potassium channel , sodium , biochemistry , artery , organic chemistry
Endothelium‐derived hyperpolarizing factor (EDHF) has recently been identified as potassium released from endothelial cells into the myo‐endothelial space. The present study was designed to test this hypothesis. In rat small mesenteric arteries, mounted in a wire myograph, relaxation to acetylcholine or potassium was not significantly changed following incubation with oxadiazolo‐quinoxalin‐1‐one (ODQ, 4 μ M ) and indomethacin (10 μ M , n =9). Maximal relaxations to acetylcholine occurred in all arteries, were maintained and were significantly greater ( P <0.01, n =9) than the transient relaxations to potassium, which only occurred in 30–40% of vessels. Removal of the vascular endothelium abolished relaxant responses both to potassium and acetylcholine ( P <0.005, n =9). Compared with responses in 5.5 m M potassium PSS, relaxation responses to added potassium in arteries maintained in 1.5 m M potassium PSS were more marked and were not dependent on the presence of an intact endothelium ( n =8). Incubation with BaCl 2 (50 μ M ) significantly inhibited the maximal relaxant response to potassium in the presence of an intact endothelium in 5.5 m M potassium PSS ( P <0.05, n =4), but had no effect on relaxation of de‐endothelialized preparations in 1.5 m M potassium PSS ( n =5). Treatment with ouabain (0.1 m M ) abolished the relaxant response to potassium in 1.5 m M potassium PSS ( P <0.001, n =9), but only partly inhibited the maximal relaxant response to acetylcholine in 5.5 m M potassium PSS ( P <0.01, n =5). These data show that at physiological concentrations of potassium an intact endothelium is necessary for potassium‐induced relaxation in rat mesenteric arteries. Furthermore, the response to potassium is clearly different to that from acetylcholine, indicating that potassium does not mimic EDHF released by acetylcholine in these arteries.British Journal of Pharmacology (2000) 129 , 605–611; doi: 10.1038/sj.bjp.0703076