Vasopressin Decreases Total Free Fatty Acids but Enhances Release of Radioactivity from Isolated Hepatocytes Labelled with [<sup>3</sup>H]Arachidonic Acid

Hughes, B P; Aj, Polverino; Lim, Filip; Gj, Barritt

doi:10.1055/s-2007-1011725

Cited by 6 publications

(3 citation statements)

References 13 publications

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“…Indirect evidence indicates that hormone-induced Ca 2+ oscillations in hepatocytes are maintained by a storeoperated Ca 2+ entry mechanism, as they are inhibited by known blockers of SOCs [19]. On the other hand, there is evidence that Ca 2+ -mobilizing hormones induce AA release [20]. The present study was designed to elucidate the effects of AA on SOCs in liver cells, and to establish whether AA activates a specific Ca 2+ conductance in these cells.…”

Section: Introductionmentioning

confidence: 98%

Arachidonic acid inhibits the store-operated Ca2+ current in rat liver cells

Rychkov

Litjens

Roberts

et al. 2005

Biochemical Journal

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Vasopressin and other phospholipase-C-coupled hormones induce oscillations (waves) of [Ca 2+ ] cyt (cytoplasmic Ca 2+ concentration) in liver cells. Maintenance of these oscillations requires replenishment of Ca 2+ in intracellular stores through Ca 2+ inflow across the plasma membrane. While this may be achieved by SOCs (storeoperated Ca 2+ channels), some studies in other cell types indicate that it is dependent on AA (arachidonic acid)-activated Ca 2+ channels. We studied the effects of AA on membrane conductance of rat liver cells using whole-cell patch clamping. We found no evidence that concentrations of AA in the physiological range could activate Ca 2+ -permeable channels in either H4IIE liver cells or rat hepatocytes. However, AA (1-10 µM) did inhibit (IC 50 = 2.4 + − 0.1 µM) Ca 2+ inflow through SOCs (I SOC ) initiated by intracellular application of Ins(1,4,5)P 3 in H4IIE cells. Preincubation with AA did not inhibit I SOC development, but decreased maximal amplitude of the current. Iso-tetrandrine, widely used to inhibit receptor-activation of phospholipase A 2 , and therefore AA release, inhibited I SOC directly in H4IIE cells. It is concluded that (i) in rat liver cells, AA does not activate an AA-regulated Ca 2+ -permeable channel, but does inhibit SOCs, and (ii) iso-tetrandrine and tetrandrine are effective blockers of CRAC (Ca 2+ -release-activated Ca 2+ ) channel-like SOCs. These results indicate that AA-activated Ca 2+ -permeable channels do not contribute to hormone-induced increases or oscillations in [Ca 2+ ] cyt in liver cells. However, AA may be a physiological modulator of Ca 2+ inflow in these cells.

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Section: Introductionmentioning

confidence: 98%

Arachidonic acid inhibits the store-operated Ca2+ current in rat liver cells

Rychkov

Litjens

Roberts

et al. 2005

Biochemical Journal

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“…In hepatocytes, arginine vasopressin has been shown to acutely stimulate release of arachidonic acid [14]. PLA 2 stimulation has also been shown to occur following exposure of hepatocytes to carbon tetrachloride [15].…”

Section: Introductionmentioning

confidence: 99%

Activation of a novel form of phospholipase A₂ during liver regeneration

1995

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Activation of phospholipase A2 (PLA2) occurs following mitogenic stimulation of cells. This study examined PLA2 activation during liver regeneration. Increased activity was detected within 1 h after partial hepatectomy, was maximal by 6 h, and returned to control levels by 24 h. Fractionation of cell-free extracts revealed multiple peaks of PLA a activity. One peak appeared identical to the previously described cPLA2, and was modestly stimulated during regeneration. A higher molecular weight form (hPLA2) was stimulated ~5-fold during regeneration. This enzyme was Ca2+-dependent and selective for arachidonoylphosphatidylethanolamine. The activation of this novel form of PLA2 represents an early event in liver regeneration, and is likely to contribute to the proliferative response.

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“…Therefore, mepacrine ap pears to be a good probe for investigating the possible role of phospholipase A2 acti vation in hormone action. The action of vaso pressin on isolated rat hepatocytes has been found to be associated with the release of arachidonic acid or its metabolites (4). We initially attempted to test whether mepacrine antagonizes vasopressin's action on [1-14C] oleate oxidation in isolated rat hepatocytes, i.e., the stimulation of 14C02 production from [1-14C] Mepacrine markedly stimulated [1-14C] oleate oxidation to 14C02 and markedly de pressed the formation of acid-soluble pro ducts (mainly ketone bodies) from [1-14C] oleate.…”

mentioning

confidence: 99%