Phasic contractions of the rat portal vein depend on intracellular Ca2+release stimulated by depolarization
| Autor: | Richard P. Burt |
|---|---|
| Rok vydání: | 2003 |
| Předmět: |
Male
medicine.medical_specialty Nifedipine Phosphodiesterase Inhibitors Physiology Pharmacology Rats Sprague-Dawley Phenylephrine chemistry.chemical_compound Chloride Channels Caffeine Physiology (medical) Internal medicine medicine Animals Vasoconstrictor Agents Cyclooxygenase Inhibitors Protein Kinase C Portal Vein Chemistry Niflumic acid Niflumic Acid Depolarization Calcium Channel Blockers Electric Stimulation Rats Electrophysiology medicine.anatomical_structure Endocrinology Vasoconstriction Potassium Calcium Calcium Channels Isotonic Solutions medicine.symptom Cardiology and Cardiovascular Medicine Intracellular Blood vessel medicine.drug |
| Zdroj: | American Journal of Physiology-Heart and Circulatory Physiology. 284:H1808-H1817 |
| ISSN: | 1522-1539 0363-6135 |
| Popis: | The phasic contraction to phenylephrine of the rat isolated portal vein was investigated using functional studies. Phasic contractions to phenylephrine and caffeine could be produced after several minutes in Ca2+-free Krebs solution, which were inhibited by cyclopiazonic acid or ryanodine. The phenylephrine and caffeine contractions were abolished, however, within 10 min in Ca2+-free Krebs solution and by nifedipine. This indicated the Ca2+stores were depleted in the absence of Ca2+influx through voltage-gated channels. The phasic contraction to phenylephrine was also abolished by niflumic acid even in Ca2+-free Krebs solution. This showed that the response depended on intracellular Ca2+release stimulated directly by depolarization, resulting from opening of Ca2+-activated Cl−channels, but did not require Ca2+influx. In support of this, K+-induced phasic contractions were also produced in Ca2+-free Krebs solution. The phenylephrine but not K+-induced phasic contractions in Ca2+-free Krebs solution were inhibited by ryanodine or cyclopiazonic acid. This would be consistent with Ca2+release from more superficial intracellular stores (affected most by these agents), probably by inositol 1,4,5-trisphospate, being required to stimulate the phenylephrine depolarization. |
| Databáze: | OpenAIRE |
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