ArticlePflugers Archiv : European journal of physiology1995
Mechanism of the ATP-induced rise in cytosolic Ca2+ in freshly isolated smooth muscle cells from human saphenous vein.
Article in Pflugers Archiv : European journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 26 citations in OpenAlex.
- Purinoreceptor-mediated current in myocytes from renal resistance arteries.British journal of pharmacology · 2010Article
- A delayed ATP-elicited K+ current in freshly isolated smooth muscle cells from mouse aorta.British journal of pharmacology · 2006Article
- Role of Rho kinase signalling in healthy and varicose human saphenous veins.British journal of pharmacology · 2002Article
- The developing relationship between receptor-operated and store-operated calcium channels in smooth muscle.British journal of pharmacology · 2002Review
- Electrophysiological properties of the bladder.International urogynecology journal and pelvic floor dysfunction · 1998Review
- Rise in cytosolic Ca2+ concentration induced by P2-purinoceptor activation in isolated myocytes from the rat gastrointestinal tract.British journal of pharmacology · 1996Article
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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
Effects of exogenous adenosine 5'-triphosphate (ATP) were studied by measurements of intracellular Ca2+ concentration ([Ca2+]i) and membrane currents in myocytes freshly isolated from the human saphenous vein. At a holding potential of -60 mV, ATP (10 microM) elicited a transient inward current and increased [Ca2+]i. These effects of ATP were inhibited by alpha,beta-methylene adenosine 5'-triphosphate (AMP-CPP, 10 microM). The ATP-gated current corresponded to a non-selective cation conductance allowing Ca2+ entry. The ATP-induced [Ca2+]i rise was abolished in Ca(2+)-free solution and was reduced to 30.1 +/- 5.5% (n = 14) of the control response when ATP was applied immediately after caffeine, and to 23.7 +/- 3.8% (n = 11) in the presence of thapsigargin. The Ca(2+)-induced Ca2+ release blocker tetracaine inhibited the rise in [Ca2+]i induced by both caffeine and ATP, with apparent inhibitory constants of 70 microM and 100 microM, respectively. Of the ATP-induced increase in [Ca2+]i 29.3 +/- 3.9% (n = 8) was tetracaine resistant. It is concluded that the effects of ATP in human saphenous vein myocytes are only mediated by activation of P2x receptor channels. The ATP-induced [Ca2+]i rise is due to both Ca2+ entry and Ca2+ release activated by Ca2+ ions that enter the cell through P2x receptor channels.
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