Effects of divalent cations on acetylcholine-evoked membrane potential in the ionophore A23187 treated mouse pancreas

Iwatsuki, Naofumi

doi:10.1007/bf00583949

Cited by 3 publications

(1 citation statement)

References 25 publications

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“…Ryanodine is known to lock the ryanodine-sensitive Ca2+ release channel in the open state in skeletal muscle (Rousseau, Smith & Meissner, 1987) and inhibit the Ca2+-dependent K+ current mediated by Ca2+ release from the intracellular store sites in smooth muscle cells (Sakai, Terada, Kitamura & Kuriyama, 1988). Low concentrations of A23187 also inhibited the Ca2+-dependent K+ current due to depletion of Ca2+ from the intracellular Ca2+ store site (Iwatsuki, 1984;Itoh, Kanmura & Kuriyama, 1985;Ohya et al 1987 b). In the present experiments ryanodine (30 /tM), A23187 (100 nM) and heparin (100 /tg/ml) did not modify the ATP-induced inward current generated by increases in the Cl-conductance in the 2-5 mM-Ca2+-TEA+ solution.…”

Section: Discussionmentioning

confidence: 99%

ATP activates cationic currents and modulates the calcium current through GTP‐binding protein in rabbit portal vein.

Xiong

Kitamura

Kuriyama

1991

The Journal of Physiology

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SUMMARY1. Effects of adenosine 5'-triphosphate (ATP) on ionic currents of dispersed smooth muscle cells of the rabbit portal vein were investigated using the voltageclamp procedure.2. ATP (> 300 ,M) produced transient and maintained inward currents. The former was inactivated within a few seconds, but the latter lasted more than several minutes. The transient but not the maintained current was blocked by pre-treatment with a,fl-methylene adenosine 5'-triphosphate (AMP-CPP). The amplitude of the latter was increased by ATP in a concentration-dependent manner. The following investigations were made on the ionic mechanism of the ATP-induced maintained inward current.3. In 2-5 mM-Ca2l-containing tetraethylammonium chloride (TEA-Cl) solution (2-5 mM-Ca2+-TEA+ solution), the reversal potential for the ATP-induced inward current was close to the Cl-equilibrium potential, and in 140 mM-Na' (nominally Ca2+-free or 0 3 mM-EGTA-containing) solution, the reversal potential was coincident with the Na+ equilibrium potential.4. In 2-5 mm-Ca2+-TEA+ solution but not in 140 mM-Na+ solution and in physiological salt solution (PSS), niflumic acid (10 pSM), a Cl-channel blocker, andCl--deficient perfusate in the pipette markedly inhibited the ATP-induced inward current. These results imply that in 2-5 mm-Ca2+-TEA+ solution the ATP-activated ion channel may admit Ca2+ which then accelerates the Ca2+-dependent Cl-current, but in 140 mM-Na+ solution and in PSS this channel may admit only Na+. 5. Intracellular perfusion of guanosine 5'-O-(3-thio triphosphate (GTPyS) did not provoke the current, but significantly increased the amplitude of the ATP-induced inward current in 2-5 mM-Ca2+-TEA+, 140 mM-Na+ and 2-5 mm-Ba2+-containing TEA+ (2-5 mM-Ba2+-TEA+) solutions. On the other hand, intracellular perfusion of guanosine 5'-O-(2-thiodiphosphate) (GDPpS) reduced the amplitude of the ATPinduced inward current in the above solutions. Z. XIONG, K. KITAMURA AND H. KURIYAMA inhibition was partly prevented by application of 20 mM-EGTA in the pipette. In 140 mM-Na' solution (with 0 3 mM-EGTA), ATP (3 mM) slightly inhibited the amplitude of the voltage-dependent inward current which was generated by permeation of the Na+ (Na+ current) through the voltage-dependent Ca2+ channel.7. In 140 mM-Na' solution (with 0-3 mM-EGTA), 2-5 mM-Ba2+-TEA+ solution and PSS, neither GTPyS nor GDP,fS in the pipette modified the amplitude of the voltage-dependent inward current. However, GTPyS pronounced but GDPflS prevented the inhibition of the voltage-dependent inward current induced by ATP. 8. Pertussis toxin (300 ng/ml) inhibited the ATP-induced inward current, and attenuated the ATP-induced inhibition of the voltage-dependent inward current in 2-5 mm-Ba2+-TEA' solution and PSS.9. These results indicate that ATP activates two different receptor-operated currents: AMP-CPP-sensitive (transient component) and -resistant (maintained component) currents. The latter appears to permeate only Na+ in PSS. The results also suggest that ATP transiently activates and then inhib...

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Section: Discussionmentioning

confidence: 99%

ATP activates cationic currents and modulates the calcium current through GTP‐binding protein in rabbit portal vein.

Xiong

Kitamura

Kuriyama

1991

The Journal of Physiology

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Cellular calcium regulates outward currents in rabbit intestinal smooth muscle cell

Ohya¹,

Kitamura²,

Kuriyama³

1987

American Journal of Physiology-Cell Physiology

100

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The nature of transient and oscillatory outward currents (ITO and IOO) in fragmented smooth muscle cells (smooth muscle ball, SMB) from the longitudinal muscle layer of the rabbit ileum, was studied using a single electrode voltage clamp technique. With a high K+ solution containing 0.3 mM ethyleneglycol-bis(beta-aminoethylether)-N,N'-tetraacetic acid (EGTA) in the pipette and physiological salt solution (PSS) in the bath, the Ca inward current was followed by a large transient outward current (ITO) and spontaneous oscillations of the outward current (IOO) on the sustained outward current (ISO) were elicited by a depolarizing pulse, positive to -30 mV (holding potential of -60 mV). When the internal fluid of the SMB was replaced with Cs+-tetraethylammonium+ (TEA+) solution, or when the concentration of EGTA in the pipette was increased to 4 mM, using the intracellular perfusion technique, both ITO and IOO were abolished. In Mn2+ solution both currents were also inhibited. Bath application of TEA+, procaine or A23187 completely blocked both ITO and IOO. Caffeine (0.3-1 mM) enhanced the amplitude of ITO and generations of IOO, and concentrations of caffeine over 3 mM transiently enhanced, but finally suppressed both these currents. These results suggest that the generation of ITO is closely related to the Ca2+ influx, whereas the generation of IOO may be initiated by an increment in the intracellular concentration of Ca2+, possibly released from store sites.

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Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

et al. 1985

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Isolated acinar cells from rat and mouse parotid glands were studied with patch-clamp whole-cell current recordings. Acetylcholine (ACh) stimulation caused a transient inward current at a membrane potential of -70 mV, and a sustained outward current at a membrane potential of 0 mV, in quasi physiological Nat, K+ ion gradients, except the zero-C1-ion gradient condition across the membrane. The reversal potential obtained from the ACh-evoked steady current was about -75 mV, in this ionic condition. When major Cl-ions of both the pipette and the bath solution were replaced, either by glutamate or by sulphate, only a large outward current was observed, at a membrane potential of -60 mV , in the presence of ACh. The addition of Cat+-ionophore A23187 caused responses similar to those evoked by ACh. The reversal potential of A23187-induced current was close to the K+ equilibrium potential of -90 mV, in a C1 -free condition. When K+-free NaCI solution was used in the pipette and the bath, A23187 caused only a large inward current, at a membrane potential of -60 mV. The reversal potential of A23187-evoked current was about -15 mV, in a symmetrical K+-free, NaCI condition. These results suggest that the ACh and A23187 activate Clr as well as K+ conducting pathways via an increase in [Ca2+]i in the parotid acinar cells. The A23187-evoked large K+ current could not be explained solely by a rise in open probability of the channels.

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Effects of divalent cations on acetylcholine-evoked membrane potential in the ionophore A23187 treated mouse pancreas

Cited by 3 publications

References 25 publications

ATP activates cationic currents and modulates the calcium current through GTP‐binding protein in rabbit portal vein.

ATP activates cationic currents and modulates the calcium current through GTP‐binding protein in rabbit portal vein.

Cellular calcium regulates outward currents in rabbit intestinal smooth muscle cell

Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

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