1991
DOI: 10.1042/bj2740243
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Cellular mechanisms of adrenaline-induced hyperpolarization in renal epitheloid MDCK cells

Abstract: The effects of adrenaline on the potential difference across the cell membrane, on formation of inositol phosphates and on intracellular Ca2+ ([Ca2+]i) were analysed in cells without or with pretreatment with pertussis toxin or phorbol 12-myristate 13-acetate (PMA). In untreated cells, adrenaline leads to a sustained hyperpolarization, a stimulation of Ins(1,4,5)P3 and Ins(1,3,4,5,)P4 formation and a transient increase in [Ca2+]i from 78 +/- 7 to 555 +/- 43 nM, followed by a plateau of 260 +/- 23 microM. In th… Show more

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Cited by 14 publications
(9 citation statements)
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References 46 publications
(30 reference statements)
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“…Phorbol esters similarly blunt the effect of bradykinin and epinephrine on IP3 formation and release of intracellular calcium (Aboolian et al, 1989;Lang et al, 1991;Pfeilschifter et al, 1991;Portilla et al, 1988a;Slivka and Insel, 1988). Thus, phorbol esters appear to generally inhibit phospholipase C. Since pretreatment with TPA blunts the ATP-induced rise of intracellular calcium both in the presence and absence of extracellular calcium, it interferes obviously with both release of intracellular calcium and entry of calcium across the cell membrane.…”
Section: Results Formation Of Inositol Phosphatesmentioning
confidence: 85%
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“…Phorbol esters similarly blunt the effect of bradykinin and epinephrine on IP3 formation and release of intracellular calcium (Aboolian et al, 1989;Lang et al, 1991;Pfeilschifter et al, 1991;Portilla et al, 1988a;Slivka and Insel, 1988). Thus, phorbol esters appear to generally inhibit phospholipase C. Since pretreatment with TPA blunts the ATP-induced rise of intracellular calcium both in the presence and absence of extracellular calcium, it interferes obviously with both release of intracellular calcium and entry of calcium across the cell membrane.…”
Section: Results Formation Of Inositol Phosphatesmentioning
confidence: 85%
“…In MDCK-cells-as in other cells (Boeynaems et al, 1988;Dubyak, 1986;Okajima et al, 1988;Tsuda et al, 1988)-the stimulation of phospholipase C involves obviously pertussis toxin sensitive G-proteins and can presumably be prevented by stimulation of protein kinase C with phorbolesters. Bradykinin, similar to ATP, activates phospholipase C in MDCK cells by a pertussis toxin sensitive mechanism (Portilla et al, 1988b;Lang et al, 1991), whereas epinephrine stimulated increase of IP3 formation is apparently not sensitive to pertussis toxin (Terman et al, 1987;Pfeilschifter et al, 1991). Obviously, phospholipase C is activated by both pertussis toxin insensitive and pertussis toxin sensitive G-proteins in MDCK cells.…”
Section: Results Formation Of Inositol Phosphatesmentioning
confidence: 95%
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“…However, in MDCK cells, pretreatment with TPA did not prevent the swellinginduced initial transient hyperpolarization of PD. Activa tion of protein kinase C by pretreatment with TPA has been shown to suppress agonist-induced formation of ino sitol phosphates due to down-regulation of phospholipase C [7][8][9], In addition, G proteins have been suggested to be involved in both RVD [32. 33] and regulatory volume increase [10].…”
Section: Discussionmentioning
confidence: 99%
“…Activation of adrenoceptors on epithelial cells triggers cascades of biochemical reactions leading to increased concentrations of intracellular second messengers like adenosine 3':5'-cyclic monophosphate (cyclic AMP) (Wong & Huang, 1990) and/or Ca2" (Pfeilschifter et al, 1991). These messengers act on different components of the secretory pathway to stimulate chloride secretion (for review see Donowitz & Welsh, 1986).…”
Section: Introductionmentioning
confidence: 99%