Intracellular alkalinization augments capacitative Ca2+ entry in vascular smooth muscle cells
Autor: | Ichiro Wakabayashi, Yoko Sotoda, Mikio Marumo |
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Rok vydání: | 2003 |
Předmět: |
medicine.medical_specialty
Serotonin Alkalosis Vascular smooth muscle Thapsigargin Time Factors Inositol Phosphates Calcium-Transporting ATPases Phosphatidylinositols Ammonium Chloride Muscle Smooth Vascular chemistry.chemical_compound Internal medicine medicine Animals Ca2 entry Aorta Cells Cultured Pharmacology Inositol monophosphate Chemistry Hydrolysis Hydrogen-Ion Concentration medicine.disease Cell biology Rats Endocrinology Vasoconstriction Verapamil Calcium Calcium Channels medicine.symptom Cardiology and Cardiovascular Medicine Intracellular alkalinization medicine.drug |
Zdroj: | Journal of cardiovascular pharmacology. 41(6) |
ISSN: | 0160-2446 |
Popis: | Agonist-induced Ca 2+ influx ofvascular smooth muscle cells is thought to be triggered by depletion of intracellular Ca 2+ stores. This study investigated the effects of intracellular alkalinization on capacitative Ca 2+ entry in A7r5 rat aortic smooth muscle cells. Intracellular alkalinization was induced by NH 4 Cl. Transplasmalemmal Ca 2+ influx due to Ca 2+ store depletion induced by thapsigargin, which was abolished by pretreatment of the cells with SKF-96365 but not affected by that with verapamil, was significantly increased by pretreatment with NH 4 Cl. Neither 5-hydroxytryptamine-induced inositol monophosphate accumulation nor intracellular Ca 2+ release from its stores was affected by NH 4 Cl. These results suggest that intracellular alkalinization acts on the process(es) after depletion of Ca 2+ stores and facilitates capacitative Ca 2+ entry in vascular smooth muscle cells. |
Databáze: | OpenAIRE |
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