ArticleBritish journal of pharmacology2006
Na+-K+-ATPase is involved in the sustained ACh-induced hyperpolarization of endothelial cells from rat aorta.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 22 citations in OpenAlex.
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- Intracellular CaPflugers Archiv : European journal of physiology · 2018Article
- The quest for endothelial atypical cannabinoid receptor: BKVascular pharmacology · 2018Article
- Direct activation of CaEuropean journal of pharmacology · 2017Article
- GPR55 agonist lysophosphatidylinositol and lysophosphatidylcholine inhibit endothelial cell hyperpolarization via GPR-independent suppression of NaVascular pharmacology · 2017Article
- Involvement of the Nonneuronal Cholinergic System in Bone Remodeling in Rat Midpalatal Suture after Rapid Maxillary Expansion.BioMed research international · 2016Article
- Endothelial atypical cannabinoid receptor: do we have enough evidence?British journal of pharmacology · 2014Review
- Na+K+-ATPase activity and K+ channels differently contribute to vascular relaxation in male and female rats.PloS one · 2014Article
- N-Arachidonoyl glycine suppresses Na⁺/Ca²⁺ exchanger-mediated Ca²⁺ entry into endothelial cells and activates BK(Ca) channels independently of GPCRs.British journal of pharmacology · 2013Article
- The GPR55 agonist lysophosphatidylinositol acts as an intracellular messenger and bidirectionally modulates Ca2+ -activated large-conductance K+ channels in endothelial cells.Pflugers Archiv : European journal of physiology · 2011Article
- GPR55-dependent and -independent ion signalling in response to lysophosphatidylinositol in endothelial cells.British journal of pharmacology · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeInhibition of Na(+)-K(+)-ATPase is known to attenuate endothelium-dependent relaxation in many arteries. The purpose of this study was to evaluate the role of Na(+)-K(+)-ATPase in the regulation of endothelial membrane potential at rest and during stimulation by ACh. EXPERIMENTAL APPROACH: Membrane potential was recorded from the endothelium of rat aorta using the perforated patch-clamp technique. KEY
resultsSuperfusion with K(+)-free solution produced a depolarization of about 11 mV from the resting value of -42.9+/-0.9 mV. Reintroduction of 4.7 mM K(+) transiently hyperpolarized endothelial cells to -52.4+/-1.8 mV and the membrane potential recovered within 10 min. Ouabain 500 microM depolarized endothelium by about 11 mV and inhibited the hyperpolarization induced by K(+) reintroduction into the K(+)-free solution. However, 500 nM ouabain did not affect the resting membrane potential or the hyperpolarization induced by K(+) reintroduction. Pre-exposure to ouabain 500 microM, but not 500 nM, attenuated the sustained component of hyperpolarization to ACh without affecting the amplitude of the transient peak hyperpolarization. In K(+)-free solution, the amplitude of peak hyperpolarization to ACh was increased, while the sustained component of hyperpolarization was attenuated. CONCLUSIONS AND IMPLICATIONS: These results indicate that electrogenic Na(+)-K(+)-ATPase partially contributes to the sustained hyperpolarization of endothelial cells from rat aorta in response to ACh. They also suggest that the alpha1, but not alpha2 or alpha3 isoforms, is involved in ACh-mediated hyperpolarization.
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