Role of endothelium and arterial K+ channels in mediating hypoxic dilation of middle cerebral arteries. Am J Physiol 1994 Aug;267(2 Pt 2):H580-6
Date
08/01/1994Pubmed ID
8067414DOI
10.1152/ajpheart.1994.267.2.H580Scopus ID
2-s2.0-0028021563 (requires institutional sign-in at Scopus site) 118 CitationsAbstract
Isolated middle cerebral arteries of rats were perfused and superfused simultaneously with physiological salt solution (PSS) equilibrated with control (21% O2) or with reduced O2 concentrations (15, 10, 5, or 0% O2). Arterial dilation in response to reduced PO2 was unaffected by the nitric oxide synthase inhibitor N omega-nitro-L-arginine (10 microM) but was inhibited by selective perfusion of the lumen with 21% O2 PSS (0% O2 in the superfusion), endothelial removal, and 1 microM indomethacin. Arterial dilation during reduced PO2 was unaffected by 1 mM tetraethylammonium to block the Ca(2+)-dependent "maxi-K+" channel but was eliminated by 1 microM glibenclamide, a blocker of the ATP-sensitive K+ channel. Glibenclamide also inhibited dilation of the vessels in response to the stable prostacyclin analogue, iloprost. The results of this study suggest that dilation of rat middle cerebral arteries in response to reduced PO2 is mediated by an endothelium-dependent cyclooxygenase product, which activates glibenclamide-sensitive K+ channels.
Author List
Fredricks KT, Liu Y, Rusch NJ, Lombard JHMESH terms used to index this publication - Major topics in bold
AnimalsCerebral Arteries
Endothelium, Vascular
Glyburide
Hypoxia
In Vitro Techniques
Male
Oxygen
Partial Pressure
Potassium Channel Blockers
Potassium Channels
Rats
Rats, Sprague-Dawley
Rest
Tetraethylammonium
Tetraethylammonium Compounds
Vasodilation
