Intracellular signalling pathways in the vasoconstrictor response of mouse afferent arterioles to adenosine
| Autor: | Torben Rene Uhrenholt, Josie P. Briggs, Pernille B. Lærkegaard Hansen, Ulla G. Friis, Jurgen Schnermann |
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| Rok vydání: | 2007 |
| Předmět: |
Boron Compounds
Intracellular Fluid Male medicine.medical_specialty Adenosine Patch-Clamp Techniques Afferent arterioles Nifedipine Pyridines Physiology Kidney Glomerulus chemistry.chemical_element Calcium-Transporting ATPases Naphthalenes Calcium Biology Calcium in biology Mice Adenosine A1 receptor Chloride Channels Internal medicine medicine Animals Inositol 1 4 5-Trisphosphate Receptors Vasoconstrictor Agents Protein Kinase C Afferent Pathways rho-Associated Kinases Voltage-dependent calcium channel Purinergic signalling Calcium Channel Blockers Amides Stimulation Chemical Glycolates Mice Inbred C57BL Perfusion Arterioles medicine.anatomical_structure Endocrinology chemistry Thapsigargin Female Endothelium Vascular medicine.symptom Vasoconstriction medicine.drug |
| Zdroj: | Hansen, P B L, Friis, U G, Uhrenholt, T R, Briggs, J & Schnermann, J 2007, ' Intracellular signalling pathways in the vasoconstrictor response of mouse afferent arterioles to adenosine ', Acta Physiologica (Print Edition), vol. 191, no. 2, pp. 89-97 . https://doi.org/10.1111/j.1748-1716.2007.01724.x |
| ISSN: | 1748-1716 1748-1708 |
| DOI: | 10.1111/j.1748-1716.2007.01724.x |
| Popis: | Udgivelsesdato: 2007-Oct AIMS: Adenosine causes vasoconstriction of afferent arterioles of the mouse kidney through activation of adenosine A(1) receptors and Gi-mediated stimulation of phospholipase C. In the present study, we further explored the signalling pathways by which adenosine causes arteriolar vasoconstriction. METHODS AND RESULTS: Adenosine (10(-7) M) significantly increased the intracellular calcium concentration in mouse isolated afferent arterioles measured by fura-2 fluorescence. Pre-treatment with thapsigargin (2 microM) blocked the vasoconstrictor action of adenosine (10(-7) M) indicating that release of calcium from the sarcoplasmic reticulum (SR), stimulated presumably by IP(3), is involved in the adenosine contraction mechanism of the afferent arteriole. In agreement with this notion is the observation that 2 aminoethoxydiphenyl borate (100 microM) blocked the adenosine-induced constriction whereas the protein kinase C inhibitor calphostin C had no effect. The calcium-activated chloride channel inhibitor IAA-94 (30 microM) inhibited the adenosine-mediated constriction. Patch clamp experiments showed that adenosine treatment induced a depolarizing current in preglomerular smooth muscle cells which was abolished by IAA-94. Furthermore, the vasoconstriction caused by adenosine was significantly inhibited by 5 microM nifedipine (control 8.3 +/- 0.2 microM, ado 3.6 +/- 0.6 microM, ado + nifedipine 6.8 +/- 0.2 microM) suggesting involvement of voltage-dependent calcium channels. CONCLUSION: We conclude that adenosine mediates vasoconstriction of afferent arterioles through an increase in intracellular calcium concentration resulting from release of calcium from the SR followed by activation of Ca(2+)-activated chloride channels leading to depolarization and influx of calcium through voltage-dependent calcium channels. |
| Databáze: | OpenAIRE |
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