Human Brain Capillary Endothelium: Modulation of K+ Efflux and K+, Ca2+ Uptake by Endothelin |
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Authors: | M Spatz N Kawai J Bembry F Lenz RM McCarron |
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Institution: | (1) Stroke Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892-4128, USA;(2) Johns Hopkins University Hospital, Baltimore, MD 21205, USA;(3) Resuscitative Medicine Program, Naval Medical Research Institute, Bethesda, MD 20889-5607, USA;(4) Stroke Branch, NINDS, National Institutes of Health, MSC 4128, Bethesda, Maryland, 20892-4128 |
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Abstract: | This report describes K+ efflux, K+ and Ca2+ uptake responses to endothelins (ET-1 and ET-3) in cultured endothelium derived from capillaries of human brain (HBEC). ET-1 dose dependently increased K+ efflux, K+ and Ca2+ uptake in these cells. ET-1 stimulated K+ efflux occurred prior to that of K+ uptake. ET-3 was ineffective. The main contributor to the ET-1 induced K+ uptake was ouabain but not bumetanide-sensitive (Na+-K+-ATPase and Na+-K+-Cl– cotransport activity, respectively). All tested paradigms of ET-1 effects in HBEC were inhibited by selective antagonist of ETA but not ETB receptors and inhibitors of phospholipase C and receptor-operated Ca2+ channels. Activation of protein kinase C (PKC) decreased whereas inhibition of PKC increased the ET-1 stimulated K+ efflux, K+ and Ca2+ uptake in HBEC. The results indicate that ET-1 affects the HBEC ionic transport systems through activation of ETA receptors linked to PLC and modulated by intracellular Ca2+ mobilization and PKC. |
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Keywords: | Human brain capillary endothelium endothelin-1 K+ efflux K+ uptake Ca2+ uptake |
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