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Effects of long-term portal hypertension on structure, active force and content of contractile and structural proteins in smooth muscle of the rat portal vein

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Summary, in English

Growth of the smooth muscle cells in the rat portal vein was induced by a partial ligation of the vessel. The ligation caused an increase in the transmural pressure and segments of the portal vein were investigated 6 weeks after the ligation. The spontaneous contractile activity of the ligated veins was similar to that of the control veins. In the ligated vessels the active force at optimal length for force development was doubled, 22.8 +/- 1.3 compared with 12.5 +/- 1.4 mN for the controls. The cross-sectional area of the media in the ligated veins, determined on transverse sections, increased from the control value of 0.10 +/- 0.01 to 0.19 +/- 0.01 mm2. Electron microscopy revealed that the mean cross-sectional area of the smooth muscle cells in the ligated portal vein was doubled (controls: 6.4 +/- 0.6, hypertrophic: 13.6 +/- 1.8 microns2). This suggests hypertrophy of the smooth muscle cells in the vessel wall as the cause for the increase in cross-sectional area of the ligated veins. An increase in the number of intermediate filaments was observed in the hypertrophied smooth muscle. The relative contents of contractile (myosin and actin) and structural (desmin and vimentin) proteins were determined with SDS-polyacrylamide gel electrophoresis. The actin/myosin and vimentin/actin ratios were unaltered by hypertrophy. The hypertrophied veins showed an increase in the desmin/actin ratio (control: 0.20 +/- 0.01, hypertrophied: 0.27 +/- 0.03). The increased amounts of desmin correlates with the increased number of intermediate filaments observed by electron microscopy.(ABSTRACT TRUNCATED AT 250 WORDS)

Publishing year

1994

Language

English

Pages

171-179

Publication/Series

Acta Physiologica Scandinavica

Volume

150

Issue

2

Document type

Journal article

Publisher

Wiley-Blackwell

Topic

  • Pharmacology and Toxicology
  • Medicinal Chemistry

Status

Published

ISBN/ISSN/Other

  • ISSN: 0001-6772