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Sustained norepinephrine contraction in the rat portal vein is lost when Ca(2+) is replaced with Sr(2+).

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Author

Summary, in English

Agonist-induced activation of smooth muscle involves a rise in intracellular Ca(2+) concentration and sensitization of myosin light chain phosphorylation to Ca(2+). Sr(2+) can enter through Ca(2+) channels, be sequestered and released from sarcoplasmic reticulum, and replace Ca(2+) in activation of myosin light chain phosphorylation. Sr(2+) cannot replace Ca(2+) in facilitation of agonist-activated Ca(2+)-dependent nonselective cation channels. It is not known whether Sr(2+) can replace Ca(2+) in small G protein-mediated sensitization of phosphorylation. To explore mechanisms involved in alpha-receptor-activated contractions in smooth muscle, effects of replacing Ca(2+) with Sr(2+) were examined in rat portal vein. Norepinephrine (NE) at

Publishing year

2002

Language

English

Pages

845-852

Publication/Series

American Journal of Physiology: Cell Physiology

Volume

282

Issue

4

Document type

Journal article

Publisher

American Physiological Society

Topic

  • Basic Medicine

Keywords

  • Smooth
  • Guanosine 5'-O-(3-Thiotriphosphate)/pharmacology
  • Muscle
  • Vascular/metabolism
  • Norepinephrine/*pharmacology
  • Portal Vein/*metabolism
  • Potassium/pharmacology
  • Rats
  • Sprague-Dawley
  • Support
  • Strontium/*pharmacokinetics
  • Non-U.S. Gov't
  • Vasoconstrictor Agents/*pharmacology
  • Vasoconstriction/drug effects/physiology
  • Female
  • Calcium/*pharmacokinetics
  • Animal

Status

Published

Research group

  • Vascular Physiology

ISBN/ISSN/Other

  • ISSN: 1522-1563