oru.sePublikasjoner
Endre søk
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf
Further studies on the interactions between the calcium mobilization and cyclic AMP pathways in guinea pig hepatocytes
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States.ORCID-id: 0000-0001-8889-5803
Vise andre og tillknytning
1986 (engelsk)Inngår i: Molecular Pharmacology, ISSN 0026-895X, E-ISSN 1521-0111, Vol. 30, nr 4, s. 315-320Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Isoproterenol (50 nM) potentiated the effects of angiotensin (1-50 nM) on 86Rb efflux and 45Ca efflux from guinea pig hepatocytes. This effect occurred in the presence or absence of extracellular Ca2+ and required the simultaneous presence of both isoproterenol and angiotensin. Neither the divalent cationophore, A23187, nor 4 beta-phorbol dibutyrate could substitute for angiotensin. The effects of isoproterenol were greatest with submaximal concentrations of angiotensin, whereas maximal concentrations of angiotensin were affected little. Isoproterenol did not substantially increase the formation of [3H]inositol triphosphate or the ratio of isomers [3H]inositol 1,4,5-trisphosphate and [3H]inositol 1,3,4-trisphosphate formed in response to angiotensin. Isoproterenol also enhanced the phase of Ca2+ mobilization involving Ca2+ entry which is consistent with the previously proposed functional linkage between receptor-regulated Ca2+ release and Ca2+ entry. These findings suggest that isoproterenol may act by increasing the sensitivity of the endoplasmic reticulum to the Ca2+-releasing action of inositol 1,4,5-trisphosphate.

sted, utgiver, år, opplag, sider
American Society for Pharmacology and Experimental Therapeutics , 1986. Vol. 30, nr 4, s. 315-320
HSV kategori
Identifikatorer
URN: urn:nbn:se:oru:diva-79019ISI: A1986E453400002PubMedID: 3020389Scopus ID: 2-s2.0-0022971690OAI: oai:DiVA.org:oru-79019DiVA, id: diva2:1386797
Merknad

Funding Agency:

United States Department of Health & Human Services

National Institutes of Health (NIH) - USA

NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK)

Appeared in article as NIADDK NIH HHS, Grant number AM-32823

Tilgjengelig fra: 2013-10-21 Laget: 2020-01-20 Sist oppdatert: 2020-01-22bibliografisk kontrollert

Open Access i DiVA

Fulltekst mangler i DiVA

PubMedScopus

Personposter BETA

Nånberg, Eewa

Søk i DiVA

Av forfatter/redaktør
Nånberg, Eewa
I samme tidsskrift
Molecular Pharmacology

Søk utenfor DiVA

GoogleGoogle Scholar

pubmed
urn-nbn

Altmetric

pubmed
urn-nbn
Totalt: 41 treff
RefereraExporteraLink to record
Permanent link

Direct link
Referera
Referensformat
  • apa
  • ieee
  • modern-language-association-8th-edition
  • vancouver
  • Annet format
Fler format
Språk
  • de-DE
  • en-GB
  • en-US
  • fi-FI
  • nn-NO
  • nn-NB
  • sv-SE
  • Annet språk
Fler språk
Utmatningsformat
  • html
  • text
  • asciidoc
  • rtf