ArticleBritish journal of pharmacology2000
A(2A) adenosine receptor mediated potassium channel activation in rat epididymal smooth muscle.
Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 17 citations in OpenAlex.
- Purinergic signaling in the male reproductive tract.Frontiers in endocrinology · 2022Review
- Function and therapeutic potential of G protein-coupled receptors in epididymis.British journal of pharmacology · 2020Review
- Plausible anti-inflammatory mechanism of resveratrol and caffeic acid against chronic stress-induced insulin resistance in mice.Inflammopharmacology · 2016Article
- SKCa Channels Blockage Increases the Expression of Adenosine A2A Receptor in Jurkat Human T Cells.BioResearch open access · 2013Article
- Role of purinergic signaling pathways in V-ATPase recruitment to apical membrane of acidifying epididymal clear cells.American journal of physiology. Cell physiology · 2010Article
- A2A adenosine receptor deficiency leads to impaired tracheal relaxation via NADPH oxidase pathway in allergic mice.The Journal of pharmacology and experimental therapeutics · 2009Article
- A1 and A2A adenosine receptor modulation of alpha 1-adrenoceptor-mediated contractility in human cultured prostatic stromal cells.British journal of pharmacology · 2004Article
- Purines and pyrimidines are not involved in NANC relaxant responses in the rabbit vaginal wall.British journal of pharmacology · 2002Article
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1 author at 1 institution in 1 country.
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Abstract
The effects of A(2) adenosine receptor agonists upon phenylephrine-stimulated contractility in preparations of rat epididymis were investigated. Preparations responded to phenylephrine (3 microM) with submaximal contractions. Adenosine and the stable agonists 5'-N-ethylcarboxamido-adenosine (NECA) and 2-p-(2-carboxyethyl) phenethylamino-N-ethylcarboxamide adenosine (CGS 21680) inhibited phenylephrine-induced contractions (potency order, NECA>CGS 21680>adenosine). The A(2A) receptor-selective antagonist, 4-(2-[7-amino-2-(2-furyl)[1,2,4]-triazolo-[2,3-a][1,3, 5]triazin-5-ylamino]ethyl)phenol (ZM 241385, 30 microM) blocked the response to NECA. The A(2A) adenosine receptor-mediated inhibitory responses to NECA were reduced by the K(ATP) channel blocker, glibenclamide (3 microM) and abolished by charybdotoxin (100 nM). The diterpene forskolin elicited a concentration-dependent inhibition of phenylephrine (3 microM)-stimulated contractility (by 62+/-8% of control at 100 microM). Charybdotoxin (100 nM), but not glibenclamide (3 microM) blocked the forskolin (10 microM) inhibition of phenylephrine-stimulated contractility. NECA elicited concentration-dependent increases in both cyclic AMP and cyclic GMP accumulation which were antagonized by ZM 241385 (30 nM). The protein kinase G activator, APT-cyclic GMP (8-(-Aminophenylthio) guanosine-3',5'-cyclic monophosphate) and the protein kinase A activator (Sp)-8-bromoadenosine-3',5'-cyclic monophosphorothioate (Sp-8-Br-cyclic AMPs), inhibited phenylephrine (3 microM) induced contractions of rat epididymis. Glibenclamide (3 microM), but not charybdotoxin (100 nM), inhibited ATP-cyclic GMP responses. Charybdotoxin (100 nM), but not glibenclamide (3 microM) reduced the effect of Sp-8-Br-cyclic AMPs. This study shows that the A(2A) adenosine receptor inhibition of epididymal contractility may be mediated through the activation of charybdotoxin- and glibenclamide-sensitive potassium channels and may involve the activation of both protein kinases A and G.
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