Vascular smooth muscle contraction evoked by cell volume modulation: Role of the cytoskeleton network

Svetlana V. Koltsova, Svetlana V. Gusakova, Yana J. Anfinogenova, Mikhail B. Baskakov, Sergei N. Orlov

Результат исследований: Материалы для журналаСтатьярецензирование

12 Цитирования (Scopus)


Previously, we reported that hyposmotic swelling evoked transient vascular smooth muscle cell (SMC) contraction that was completely abolished by L-type Ca2+ channel blockers. In contrast, sustained contraction revealed in hyper- and isoosmotically-shrunken SMCs was insensitive to L-type channel blockers and was diminished in Ca2+-free medium by only 30-50%. Several research groups reported cell volume-dependent cytoskeleton network rearrangements. This study examines the role of cytoskeleton proteins in cell volume-dependent contraction of endothelium-denuded vascular smooth muscle rings (VSMR) from the rat thoracic aorta. Hyperosmotic shrinkage and hyposmotic swelling were triggered by modulation of medium osmolality; isosmotic shrinkage was induced by VSMR transfer from hypo- to isosmotic medium. The relative content of globular (G) and fibrillar (F) actin was estimated by fluorescence microscopy. Hyperosmotic shrinkage and hyposmotic swelling led to elevation of the F-actin/G-actin ratio by 2.5- and 1.8-fold respectively. Contraction of shrunken and swollen VSMR was insensitive to modulators of microtubules such as vinblastine, colchicine and docetaxel. Microfilament disassembly by cytochalasin B resulted in dramatic attenuation of the maximal amplitude of contraction of hyperosmotically-shrunken and hyposmotically-swollen VSMR, and almost completely abolished the contraction triggered by isosmotic shrinkage. These data suggest that both L-type Ca2+ channel-mediated contraction of swollen vascular SMC and Ca2+ o-insensitive contractions of shrunken cells are triggered by reorganization of the microfilament network caused by elevation of the F-actin/G-actin ratio.

Язык оригиналаАнглийский
Страницы (с-по)29-36
Число страниц8
ЖурналCellular Physiology and Biochemistry
Номер выпуска1-3
СостояниеОпубликовано - 2008
Опубликовано для внешнего пользованияДа

ASJC Scopus subject areas

  • Physiology
  • Cell Biology

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