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
Avdelning/ar
Publiceringsår
2002
Språk
Engelska
Sidor
845-852
Publikation/Tidskrift/Serie
American Journal of Physiology: Cell Physiology
Volym
282
Issue
4
Länkar
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