The interaction of intracellular Mg2+ and pH on Cl- fluxes associated with intracellular pH regulation in barnacle muscle fibers.

Russell, J. M.; Brodwick, Malcolm S.

doi:10.1085/jgp.91.4.495

Cited by 17 publications

(4 citation statements)

References 37 publications

(61 reference statements)

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“…Fourth, the inhibiting effect of injected Mg2+ may not be limited to the Ca2+ release channel of the SR. It may include inhibition of the Na+/HCO3--Cl-/H+ exchanger in the light of evidence that a fall in internal pMg in barnacle fibres inhibits the SITS-or DIDS-sensitive Cl-effluxes and net acid extrusion (Russell & Brodwick, 1988). And fifth, it is notable that the magnitude of the response of fibres suspended in Li+-ASW to the injection of PD is virtually the same as that of fibres suspended in Na+-ASW.…”

Section: Discussionmentioning

confidence: 98%

A study of the ouabain‐insensitive sodium efflux in barnacle muscle fibres using phorbol dibutyrate as a probe.

Bittar

Nwoga

1990

The Journal of Physiology

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SUMMARY1. The resting ouabain-insensitive Na+ efflux in muscle fibres isolated from the barnacle, Balanus nubilus, is stimulated by external or internal application of phorbol 12,13-dibutyrate (PD). The response occurs fairly promptly and may not decay at all, or more commonly, decay rather slowly. The magnitude of the response to external or internal application of PD is dose-dependent, the minimum effective concentration being about 10-8 M.2. The response to PD fails to occur in the nominal absence of external Ca2+. Sudden removal of external Ca subsequent to peak stimulation by PD leads to almost complete reversal of the response. The response to PD of fibres suspended in Li+-ASW (artificial sea water) is similar in magnitude to that of fibres suspended in Na+-ASW. However, it differs in that it is of a sustained nature.3. Calcium channel blockers, e.g. verapamil, completely prevent the response to PD from occurring. Both Cd2+ and Co2+ are less effective than verapamil.4. Pre-but not post-injection of EGTA reduces the response to PD. Pre-or postinjection of Mg2+ reduces the response considerably.5. Fibres pre-injected with GTP show a reduced response to PD. Fibres preinjected with PD show a reduced response to GTP. Pre-injection of protein kinase inhibitor is without effect on the response to PD.6. Furosemide, piretanide and bumetanide are without effect on the response to PD. 7. DIDS (4,4'-diisothiocyanostilbene-2,2-disulphonic acid) is a potent inhibitor of the response to PD but not amiloride. Pyridoxal 5-phosphate and benzolamide are also powerful inhibitors. Pyridoxal 5-phosphate in combination with benzolamide fails to completely abolish or reverse the response to PD.8. Luminescence from aequorin is promptly increased by PD in a dose-dependent manner, the minimal effective concentration being in the nanomolar range. The signal is monophasic or multiphasic in shape, and is often less than 5 min in duration. Not infrequently, however, the aequorin response fails to completely decay and the new level of resting glow remains above the original baseline level.9. Collectively, these observations accord with a tentative general hypothesis stating that the stimulatory response of the ouabain-insensitive Na+ efflux to PD is triggered by two mechanisms. One involves a rise in myoplasmic free [Ca2+] resulting MS 7690 E2 E. BITTAR AND J. NWOGA from the entry of external Ca2+ via opened Ca2+ channels which is followed by the operation of the Na+{-Ca2+ exchanger in the reverse mode. The other involves stimulation of the Na+/HCO3--Cl-/H+ exchanger, presumably as the result of phosphorylation and/or an internal acidosis brought about by a sufficient rise in myoplasmic free [Ca2+].

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Section: Discussionmentioning

confidence: 98%

A study of the ouabain‐insensitive sodium efflux in barnacle muscle fibres using phorbol dibutyrate as a probe.

Bittar

Nwoga

1990

The Journal of Physiology

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“…Such an interaction has a strong chemical basis and was previously reported in various studies. For example, Russell and Brodwick ( 1988 ) demonstrated that competition of H + and Mg 2+ ions can affect Cl − fluxes in giant barnacle muscle cells. Mg 2+ and pH i interaction was also demonstrated for TRPM7 cation channels (Jiang et al, 2005 ) or P2X7 receptors (Acuña-Castillo et al, 2007 ).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Connexin-36 Gap Junction Channels by Intracellular pH and Magnesium Ions

et al. 2018

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Connexin-36 (Cx36) protein forms gap junction (GJ) channels in pancreatic beta cells and is also the main Cx isoform forming electrical synapses in the adult mammalian brain. Cx36 GJs can be regulated by intracellular pH (pHi) and cytosolic magnesium ion concentration ([Mg2+]i), which can vary significantly under various physiological and pathological conditions. However, the combined effect and relationship of these two factors over Cx36-dependent coupling have not been previously studied in detail. Our experimental results in HeLa cells expressing Cx36 show that changes in both pHi and [Mg2+]i affect junctional conductance (gj) in an interdependent manner; in other words, intracellular acidification cause increase or decay in gj depending on whether [Mg2+]i is high or low, respectively, and intracellular alkalization cause reduction in gj independently of [Mg2+]i. Our experimental and modelling data support the hypothesis that Cx36 GJ channels contain two separate gating mechanisms, and both are differentially sensitive to changes in pHi and [Mg2+]i. Using recombinant Cx36 we found that two glutamate residues in the N-terminus could be partly responsible for the observed interrelated effect of pHi and [Mg2+]i. Mutation of glutamate at position 8 attenuated the stimulatory effect of intracellular acidification at high [Mg2+]i, while mutation at position 12 and double mutation at both positions reversed stimulatory effect to inhibition. Moreover, Cx36*E8Q lost the initial increase of gj at low [Mg2+]i and double mutation lost the sensitivity to high [Mg2+]i. These results suggest that E8 and E12 are involved in regulation of Cx36 GJ channels by Mg2+ and H+ ions.

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“…Thus, the total time for dialysis was ∼80–90 min. Previous work has shown that 60–90 min is sufficient for either 22 Na ( Russell et al, 1983 ) or 36 Cl ( Boron et al, 1978 ; Russell and Brodwick, 1988 ) in the DF to achieve isotopic equilibrium. After dialysis was halted, pH i was allowed to stabilize for ∼15 min in a Na + -free ASW.…”

Section: Methodsmentioning

confidence: 99%

Intracellular Cl− Dependence of Na-H Exchange in Barnacle Muscle Fibers under Normotonic and Hypertonic Conditions

Hogan

Davis

Boron

1997

The Journal of General Physiology

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We previously showed that shrinking a barnacle muscle fiber (BMF) in a hypertonic solution (1,600 mosM/kg) stimulates an amiloride-sensitive Na-H exchanger. This activation is mediated by a G protein and requires intracellular Cl−. The purpose of the present study was to determine (a) whether Cl− plays a role in the activation of Na-H exchange under normotonic conditions (975 mosM/kg), (b) the dose dependence of [Cl−]i for activation of the exchanger under both normo- and hypertonic conditions, and (c) the relative order of the Cl−- and G-protein-dependent steps. We acid loaded BMFs by internally dialyzing them with a pH-6.5 dialysis fluid containing no Na+ and 0–194 mM Cl−. The artificial seawater bathing the BMF initially contained no Na+. After dialysis was halted, adding 50 mM Na+ to the artificial seawater caused an amiloride-sensitive pHi increase under both normo- and hypertonic conditions. The computed Na-H exchange flux (J Na-H) increased with increasing [Cl−]i under both normo- and hypertonic conditions, with similar apparent K m values (∼120 mM). However, the maximal J Na-H increased by nearly 90% under hypertonic conditions. Thus, activation of Na-H exchange at low pHi requires Cl− under both normo- and hypertonic conditions, but at any given [Cl−]i, J Na-H is greater under hyper- than normotonic conditions. We conclude that an increase in [Cl−]i is not the primary shrinkage signal, but may act as an auxiliary shrinkage signal. To determine whether the Cl−-dependent step is after the G-protein-dependent step, we predialyzed BMFs to a Cl−-free state, and then attempted to stimulate Na-H exchange by activating a G protein. We found that, even in the absence of Cl−, dialyzing with GTPγS or AlF3, or injecting cholera toxin, stimulates Na-H exchange. Because Na-H exchange activity was absent in control Cl−-depleted fibers, the Cl−-dependent step is at or before the G protein in the shrinkage signal-transduction pathway. The stimulation by AlF3 indicates that the G protein is a heterotrimeric G protein.

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The interaction of intracellular Mg2+ and pH on Cl- fluxes associated with intracellular pH regulation in barnacle muscle fibers.

Cited by 17 publications

References 37 publications

A study of the ouabain‐insensitive sodium efflux in barnacle muscle fibres using phorbol dibutyrate as a probe.

A study of the ouabain‐insensitive sodium efflux in barnacle muscle fibres using phorbol dibutyrate as a probe.

Modulation of Connexin-36 Gap Junction Channels by Intracellular pH and Magnesium Ions

Intracellular Cl− Dependence of Na-H Exchange in Barnacle Muscle Fibers under Normotonic and Hypertonic Conditions

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