ArticleRespiratory research2005
Multiple P2Y receptors couple to calcium-dependent, chloride channels in smooth muscle cells of the rat pulmonary artery.
Article in Respiratory research, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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11 citing papers in PubMed, 27 citations in OpenAlex.
- How selective antagonists and genetic modification have helped characterise the expression and functions of vascular P2Y receptors.Purinergic signalling · 2025Review
- Purinergic regulation of pulmonary vascular tone.Purinergic signalling · 2024Review
- Characterisation of P2Y receptor subtypes mediating vasodilation and vasoconstriction of rat pulmonary artery using selective antagonists.Purinergic signalling · 2022Article
- Purinergic Signaling During Hyperglycemia in Vascular Smooth Muscle Cells.Frontiers in endocrinology · 2020Review
- Extract ofJournal of traditional and complementary medicine · 2019Article
- A critical look at the function of the P2Y11 receptor.Purinergic signalling · 2016Review
- Novel vasocontractile role of the P2Y₁₄ receptor: characterization of its signalling in porcine isolated pancreatic arteries.British journal of pharmacology · 2014Article
- Administration of exogenous adenosine triphosphate to ischemic skeletal muscle induces an energy-sparing effect: role of adenosine receptors.The Journal of surgical research · 2013Article
- A Ca²⁺-dependent chloride current and Ca²⁺ influx via Ca(v)1.2 ion channels play major roles in P2Y receptor-mediated pulmonary vasoconstriction.British journal of pharmacology · 2012Article
- Characterization of P2Y receptor subtypes functionally expressed on neonatal rat cardiac myofibroblasts.British journal of pharmacology · 2009Article
- Interaction of P2 purinergic receptors with cellular macromolecules.Naunyn-Schmiedeberg's archives of pharmacology · 2008Review
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3 authors at 1 institution in 2 countries.
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Abstract
backgroundUridine 5'-triphosphate (UTP) and uridine 5'-diphosphate (UDP) act via P2Y receptors to evoke contraction of rat pulmonary arteries, whilst adenosine 5'-triphosphate (ATP) acts via P2X and P2Y receptors. Pharmacological characterisation of these receptors in intact arteries is complicated by release and extracellular metabolism of nucleotides, so the aim of this study was to characterise the P2Y receptors under conditions that minimise these problems.
methodsThe perforated-patch clamp technique was used to record the Ca2+-dependent, Cl- current (I(Cl,Ca)) activated by P2Y receptor agonists in acutely dissociated smooth muscle cells of rat small (SPA) and large (LPA) intrapulmonary arteries, held at -50 mV. Contractions to ATP were measured in isolated muscle rings. Data were compared by Student's t test or one way ANOVA.
resultsATP, UTP and UDP (10(-4) M) evoked oscillating, inward currents (peak = 13-727 pA) in 71-93% of cells. The first current was usually the largest and in the SPA the response to ATP was significantly greater than those to UTP or UDP (P < 0.05). Subsequent currents tended to decrease in amplitude, with a variable time-course, to a level that was significantly smaller for ATP (P < 0.05), UTP (P < 0.001) and UDP (P < 0.05) in the SPA. The frequency of oscillations was similar for each agonist (mean approximately to 6-11.min(-1)) and changed little during agonist application. The non-selective P2 receptor antagonist suramin (10(-4) M) abolished currents evoked by ATP in SPA (n = 4) and LPA (n = 4), but pyridoxalphosphate-6-azophenyl-2',4'-disulphonic acid (PPADS) (10(-4) M), also a non-selective P2 antagonist, had no effect (n = 4, 5 respectively). Currents elicited by UTP (n = 37) or UDP (n = 14) were unaffected by either antagonist. Contractions of SPA evoked by ATP were partially inhibited by PPADS (n = 4) and abolished by suramin (n = 5). Both antagonists abolished the contractions in LPA.
conclusionAt least two P2Y subtypes couple to ICl,Ca in smooth muscle cells of rat SPA and LPA, with no apparent regional variation in their distribution. The suramin-sensitive, PPADS-resistant site activated by ATP most resembles the P2Y11 receptor. However, the suramin- and PPADS-insensitive receptor activated by UTP and UDP does not correspond to any of the known P2Y subtypes. These receptors likely play a significant role in nucleotide-induced vasoconstriction.
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