Calcium movements in in situ mitochondria following activation of α‐adrenergic receptors in rat liver cells

Poggioli, J; Berthon, B; Claret, M

doi:10.1016/0014-5793(80)81178-1

Cited by 71 publications

(41 citation statements)

References 18 publications

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“…This could have occurred if the reduction in the electrochemical gradient for Ca*+ had promoted a net similar time courses [8,9]. In contrast, the o-adrenoreceptor agonist isoprenaline (0.05-0.2 PM) had no apparent effect on the Na+-K* pump in these cells (G. M. B., unpublished).…”

Section: Resultsmentioning

confidence: 92%

The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes

et al. 1982

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Section: Resultsmentioning

confidence: 92%

The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes

et al. 1982

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“…Two quite different hypotheses are under consideration. One view is that Ca2+ is released from stores associated with the cell membrane, and perhaps also the associated endoplasmic reticulum (Althaus-Saltzmann et al, 1980;Poggioli et al, 1980;Burgess et al, 1983). Others (see Williamson et al, 1981 andExton, 1981 for references and further discussion) have concluded that the mitochondria are an important primary source from which Type 1 receptors, acting through an as yet unidentified intermediate, initiate the release of Ca2+.…”

Section: Ij 51 Discussionmentioning

confidence: 99%

Interactions between receptors that increase cytosolic calcium and cyclic AMP in guinea‐pig liver cells

Cocks

Jenkinson

Koller

1984

British J Pharmacology

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1 The action of agonists which increase the K+ permeability of liver cells was studied by using a K+-sensitive electrode to record the net movement of K+ between guinea-pig isolated hepatocytes and their suspension medium. 2 Two types of agonist were examined. Type 1 comprised angiotensin II, ATP, noradrenaline and amidephrine, all of which are thought to raise cytosolic Ca2+ in hepatocytes. The Type 2 agonists were isoprenaline and glucagon, which activate adenylate cyclase. 3 Each type of agonist initiated K+ loss from the hepatocytes though the response to Type 2 agonists was more variable than that to Type 1, and sometimes absent. 4 Simultaneous application of a small concentration of an agonist from each class caused a loss of K+ which was much larger than the sum of that seen with each agonist alone, i.e. potentiation occurred.5 The a-adrenoceptor antagonist, WB 4101, abolished potentiation if applied after an cx-agonist, and before a Type 2 agonist, showing that both receptors have to be active for potentiation to occur. 6 Simultaneous application of a maximal concentration of each type of agonist caused a larger loss of K+ (-17% of the cell total within 45 s) than did a maximal concentration of a Type 1 agonist alone (~10%). 7 Since the K+ loss caused by these agonists is thought to be a consequence of a rise in cytosolic Ca2 , the influence of both types of agonist on 45Ca and 42K efflux from guinea-pig liver slices was studied.8 The effect of isoprenaline on 45Ca and 42K efflux became much greater following a previous application of the oa-adrenoceptor agonist, amidephrine. 9 In the presence of apamin, the potentiated effect of isoprenaline on 42K efflux was greatly reduced whereas that on 45Ca efflux was little affected. 10 The effects of Type 1 and Type 2 agonists separately and together on the cyclic AMP content of isolated hepatocytes were examined. Type 2 agonists increased cyclic AMP in the expected way. The increase became slightly smaller, if anything, when a Type 1 agonist was applied at the same time. Hence potentiation could not be ascribed to changes in cyclic AMP formation. 11 Possible mechanisms for potentiation are discussed. Our evidence suggests, albeit indirectly, that it is a consequence of an interaction between the effects of the two types of agonist on cytosolic c2+.

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“…Alternatively, the endoplasmic reticulum may be the source of the Ca (Poggioli et al 1980). In the same vein, there is little to indicate the directness of the influence of cytosolic Ca on K permeability: one of the Ca-dependent regulatory proteins exemplified by calmodulin (see the reviews by Cheung, 1980; Klee, Crouch & Richman, 1980;and Means & Dedman, 1980) …”

Section: G M Burgess M Claret and D H Jenkinsonmentioning

confidence: 99%

Effects of quinine and apamin on the calcium‐dependent potassium permeability of mammalian hepatocytes and red cells.

Burgess¹,

Claret²,

Jenkinson³

1981

The Journal of Physiology

283

181

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SUMMARY1. K-sensitive electrodes placed in the extracellular fluid have been used to show that ATP and noradrenaline cause a rapid loss of up to 10 % of the K content of isolated guinea-pig hepatocytes.2. The hypothesis that this response is a consequence of a rise in the K permeability of the hepatocyte membrane triggered by an increase in cytosolic Ca is supported by the finding that the divalent cation ionophore A23187 also initiated K loss, in this instance of up to 20-25 % of the amount in the cells.3. Under similar conditions A23187 caused a transient increase, followed by a larger decrease, in the 45Ca content of guinea-pig hepatocytes equilibrated with this isotope. The decrease alone was seen with ATP and noradrenaline.4. Quinine (1 mM) and the bee venom neurotoxin apamin (10 nM) greatly reduced the effect of ATP, noradrenaline and A23187 on K content without affecting the changes in 45Ca movement.5. Apamin (10 nM) also abolished the increase in 42K efflux which follows the application of the a-adrenoceptor agonist amidephrine to rabbit liver slices; the concurrent rises in 45Ca efflux and glucose release were unaffected.6. It was concluded that quinine and apamin are able to block either the Ca-dependent K channels present in guinea-pig and rabbit liver cell membranes or the mechanism that controls them.7. Surprisingly, rat hepatocytes took up rather than lost K when treated with the concentrations of ATP, noradrenaline or A23187 that initiated K loss from guinea-pig cells. This response was greatly reduced by ouabain.8. Application of large concentrations of A23187 to rat hepatocytes caused K loss associated with cell death.9. The influence of apamin (10-1000 nM) and quinine (200-1000 UM) on the Ca-dependent K permeability of red blood cells and ghosts was also studied. Apamin was without effect even when applied to both sides of the ghost membrane, whereas quinine caused inhibition, as reported by others.10. The results suggest that Ca-dependent K channels or carriers are present in

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Calcium movements in in situ mitochondria following activation of α‐adrenergic receptors in rat liver cells

Cited by 71 publications

References 18 publications

The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes

The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes

Interactions between receptors that increase cytosolic calcium and cyclic AMP in guinea‐pig liver cells

Effects of quinine and apamin on the calcium‐dependent potassium permeability of mammalian hepatocytes and red cells.

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Calcium movements in in situ mitochondria following activation of α‐adrenergic receptors in rat liver cells

Cited by 71 publications

References 18 publications

The effect of Ca2+‐mobilising hormones on the Na+‐K+ pump in isolated rat liver hepatocytes

The effect of Ca2+‐mobilising hormones on the Na+‐K+ pump in isolated rat liver hepatocytes

Interactions between receptors that increase cytosolic calcium and cyclic AMP in guinea‐pig liver cells

Effects of quinine and apamin on the calcium‐dependent potassium permeability of mammalian hepatocytes and red cells.

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Product

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The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes

The effect of Ca²⁺‐mobilising hormones on the Na⁺‐K⁺ pump in isolated rat liver hepatocytes