Norepinephrine-induced loss of phosphatidylinositol from isolated rat liver plasma membrane Effects of divalent cations

AbstractNorepinephrine at 5 μM induces a rapid (60 s) and specific loss of phosphatidylinositol (PtdIns) when added to isolated rat liver plasma membranes. The hormone action is inhibited by the α-adrenergic antagonist phentolamine (20 μM). Depletion of Mg2+ and Ca2+ singly or in combination from the incubation buffer mimicks the hormone effect on PtdIns breakdown. No further effect on PtdIns degradation could be measured when norepinephrine was added to the cation-depleted buffers. Addition of the Ca2+ ionophore A23187 to the isolated membranes has no effect. It is concluded that PtdIns degradation can be provoked in isolated rat liver plasma membrane through α-adrenergic receptor activation and that this effect is dependent on divalent cations in the sense that loss of cations from the membrane allows degradation to commence

1.Régulation de l'échangeur Na/H isoforme 3 (NHE) en conditions physiologiques et physiopathologiques (rôle du cytosquelette d'actine - Effet de l'angiotensine II. 2. Identification de NHE3 comme biomarqueur urinaire de l'insuffisance rénale aigue)

PARIS-BIUSJ-Thèses (751052125) / SudocPARIS-BIUSJ-Physique recherche (751052113) / SudocSudocFranceF

Investigation of the the roles of Ca2+ and InsP3 diffusion in the coordination of Ca2+ signals between connected hepatocytes

Glycogenolytic agonists induce coordinated Ca(2+) oscillations in multicellular rat hepatocyte systems as well as in the intact liver. The coordination of intercellular Ca(2+) signals requires functional gap-junction coupling. The mechanisms ensuring this coordination are not precisely known. We investigated possible roles of Ca(2+) or inositol 1,4,5-trisphosphate (InsP(3)) as a coordinating messengers for Ca(2+) spiking among connected hepatocytes. Application of ionomycin or of supra-maximal concentrations of agonists show that Ca(2+) does not significantly diffuse between connected hepatocytes, although gap junctions ensure the passage of small signaling molecules, as demonstrated by FRAP experiments. By contrast, coordination of Ca(2+) spiking among connected hepatocytes can be favored by a rise in the level of InsP(3), via the increase of agonist concentrations, or by a shift in the affinity of InsP(3) receptor for InsP(3). In the same line, coordination cannot be achieved if the InsP(3) is rapidly metabolized by InsP(3)-phosphatase in one cell of the multiplet. These results demonstrate that even if small amounts of Ca(2+) diffuse across gap junctions, they most probably do not play a significant role in inducing a coordinated Ca(2+) signal among connected hepatocytes. By contrast, coordination of Ca(2+) oscillations is fully dependent on the diffusion of InsP(3) between neighboring cells.info:eu-repo/semantics/publishe