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Further studies on the interactions between the calcium mobilization and cyclic AMP pathways in guinea pig hepatocytes

Burgess, G.M. (författare)
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
Dooley, R.K. (författare)
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
McKinney, J.S. (författare)
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
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Nånberg, Eewa, 1957- (författare)
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States,Uppsala universitet, Medicinska vetenskapsområdet, Medicinska fakulteten, Institutionen för genetik och patologi
Putney, J.W. Jr (författare)
Division of Cellular Pharmacology, Medical College of Virginia, Richmond, VA 23298, United States
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 (creator_code:org_t)
American Society for Pharmacology and Experimental Therapeutics, 1986
1986
Engelska.
Ingår i: Molecular Pharmacology. - : American Society for Pharmacology and Experimental Therapeutics. - 0026-895X .- 1521-0111. ; 30:4, s. 315-320
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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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.

Ämnesord

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Fysiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Physiology (hsv//eng)

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