ArticlePflugers Archiv : European journal of physiology1994
Alpha 2-adrenoceptors activate dihydropyridine-sensitive calcium channels via Gi-proteins and protein kinase C in rat portal vein myocytes.
Article in Pflugers Archiv : European journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 40 citations in OpenAlex.
- Novel drug treatments for pain in advanced cancer and serious illness: a focus on neuropathic pain and chemotherapy-induced peripheral neuropathy.Palliative care and social practice · 2024Review
- Mechanism of asynchronous Ca(2+) waves underlying agonist-induced contraction in the rat basilar artery.British journal of pharmacology · 2009Article
- Lysophosphatidylcholine Increases Ca Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2008Article
- Agonist trafficking of G(i/o)-mediated alpha(2A)-adrenoceptor responses in HEL 92.1.7 cells.British journal of pharmacology · 2001Article
- Different subtypes of alpha 1A-adrenoceptor mediating contraction of rat epididymal vas deferens, rat hepatic portal vein and human prostate distinguished by the antagonist RS 17053.British journal of pharmacology · 1996Article
- Angiotensin II-activated Ca2+ entry-induced release of Ca2+ from intracellular stores in rat portal vein myocytes.British journal of pharmacology · 1996Article
- A Gi1-2-protein is required for alpha 2A-adrenoceptor-induced stimulation of voltage-dependent Ca2+ channels in rat portal vein myocytes.Pflugers Archiv : European journal of physiology · 1995Article
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Authors and funding
2 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The presence of functional alpha 2-adrenoceptors was investigated in isolated smooth muscle cells from rat portal vein using the nystatin-perforated patch-clamp technique. The free cytoplasmic calcium concentration ([Ca2+]i) was estimated using emission from the dye Fura-2. Activation of alpha 2-adrenoceptors by clonidine (an alpha 2-adrenoceptor agonist) or noradrenaline (a non-selective alpha-adrenoceptor agonist), both in the presence of 0.1 microM prazosin to block alpha 1-adrenoceptors, caused a slow and sustained increase in [Ca2+]i which was inhibited by 0.1 microM rauwolscine (an alpha 2-adrenoceptor antagonist). A similar Ca2+ response was obtained with oxymetazoline (a selective alpha 2A-adrenoceptor agonist) suggesting that the increase in [Ca2+]i resulted from activation of the alpha 2A-adrenoceptor subtype. The increase in [Ca2+]i did not occur in calcium-free solution or in the presence of oxodipine (a voltage-dependent calcium channel blocker), indicating that it depended on a calcium influx. The alpha 2A-adrenoceptor-activated calcium influx was unchanged after complete release of the stored calcium induced by applications of ryanodine and caffeine. In addition, no accumulation of inositol trisphosphate was detected in the presence of 0.1 microM prazosin. Taken together, these results indicate that alpha 2A-adrenoceptor activation does not stimulate phosphoinositide turnover and subsequent calcium release from intracellular stores. Whole-cell patch-clamp experiments showed that alpha 2A-adrenoceptor activation promoted calcium influx through voltage-dependent L-type channels.(ABSTRACT TRUNCATED AT 250 WORDS)
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