Search: id:"swepub:oai:DiVA.org:oru-79019" >
Further studies on ...
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Burgess, G.M.Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
(author)
Further studies on the interactions between the calcium mobilization and cyclic AMP pathways in guinea pig hepatocytes
- Article/chapterEnglish1986
Publisher, publication year, extent ...
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American Society for Pharmacology and Experimental Therapeutics,1986
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:oru-79019
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https://urn.kb.se/resolve?urn=urn:nbn:se:oru:diva-79019URI
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https://urn.kb.se/resolve?urn=urn:nbn:se:kau:diva-29823URI
Supplementary language notes
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Language:English
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Summary in:English
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Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Funding Agency:United States Department of Health & Human ServicesNational Institutes of Health (NIH) - USANIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK)Appeared in article as NIADDK NIH HHS, Grant number AM-32823
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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.
Subject headings and genre
Added entries (persons, corporate bodies, meetings, titles ...)
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Dooley, R.K.Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
(author)
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McKinney, J.S.Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
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Nånberg, Eewa,1957-Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States,Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi(Swepub:kau)eewanan
(author)
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Putney, J.W.JrDivision of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
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Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United StatesUppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi
(creator_code:org_t)
Related titles
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In:Molecular Pharmacology: American Society for Pharmacology and Experimental Therapeutics30:4, s. 315-3200026-895X1521-0111
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