Webbläsaren som du använder stöds inte av denna webbplats. Alla versioner av Internet Explorer stöds inte längre, av oss eller Microsoft (läs mer här: * https://www.microsoft.com/en-us/microsoft-365/windows/end-of-ie-support).

Var god och använd en modern webbläsare för att ta del av denna webbplats, som t.ex. nyaste versioner av Edge, Chrome, Firefox eller Safari osv.

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

Författare

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

Publiceringsår

2002

Språk

Engelska

Sidor

845-852

Publikation/Tidskrift/Serie

American Journal of Physiology: Cell Physiology

Volym

282

Issue

4

Dokumenttyp

Artikel i tidskrift

Förlag

American Physiological Society

Ämne

  • Basic Medicine

Nyckelord

  • 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

Forskningsgrupp

  • Vascular Physiology

ISBN/ISSN/Övrigt

  • ISSN: 1522-1563