J. Van De Voorde et B. Vanheel, EDHF-mediated relaxation in rat gastric small arteries: Influence of ouabain/Ba2+ and relation to potassium ions, J CARDIO PH, 35(4), 2000, pp. 543-548
Citations number
26
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
In several blood vessels, endothelium-dependent vasorelaxation is in part m
ediated by an endothelium-derived hyperpolarizing factor (EDHF), the nature
of which is as yet unknown. Experiments were performed to investigate whet
her the recently raised hypothesis that EDHF might be identified as the pot
assium ion, released by activation of endothelial K-Ca channels and inducin
g relaxation by stimulation of Na+/K(+)pump and the inward rectifier K+ con
ductance, might be valid for small rat gastric arteries. EDHF-induced relax
ation (assessed as the nitro-L-arginine/indomethacin resistant component of
acetylcholine-induced relaxation), but not nitroprusside-induced relaxatio
n is strongly inhibited in the presence of ouabain (0.5 mM)/Ba2+ (30 mu M),
ouabain being responsible for the greater part of the inhibition. This inh
ibition is reversible. Application of increasing concentrations of K+ elici
ts transient relaxations in some preparations, but in a greater part of the
preparations, no or only small relaxations. In membrane potential measurem
ents, it was found that increasing concentrations of extracellular K+ consi
stently depolarized smooth muscle cells, whereas acetylcholine elicits hype
rpolarization. The K-Ca channel openers NS 1619 and 1-EBIO elicit relaxatio
n effects that are not diminished after removal of the endothelium and are
not inhibited by ouabain/Ba2+. It is concluded that EDHF-mediated relaxatio
n is sensitive to inhibition by ouabain/Ba2+ but that the relation of this
inhibitory influence to an action of K+ as EDHF is uncertain.