scholarly journals Elecropharmacology of Taurine on the Hyperpolarization-Activated Inward Current and the Sustained Inward Current in Spontaneously Beating Rat Sino-Atrial Nodal Cells

2003 ◽  
Vol 91 (3) ◽  
pp. 229-238 ◽  
Author(s):  
Hiroyasu Satoh
Keyword(s):  
Inward Current ◽  
Sustained Inward Current

Voltage-dependent calcium current and the effects of adrenergic modulation in rat aortic smooth muscle cells

1992 ◽  
Vol 337 (1279) ◽  
pp. 37-47 ◽  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Ca Channel ◽  
Ca Current ◽  
Inward Current ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle ◽  
Inward Currents ◽  
Sustained Inward Current

Smooth muscle cells from rat aorta were cultured in defined, serum-free medium and studied using whole-cell patch-clamp techniques. Under conditions designed to isolate currents through Ca channels, step depolarizations produced inward currents which were fast in onset and inactivated rapidly, with little sustained inward current being observed. Both Ni and Cd blocked these currents, with Ni being effective at 50 μM. Removal of external Na or addition of 1 μM tetrodotoxin had no effect. Peak inward currents were attained at about —15 mV, with half-maximal activation at —41 mV using —80 mV holding potentials. The transient inward currents were reduced by depolarized holding potentials, with half-maximal steady-state inactivation at —48 mV. In three of the 98 cells studied, small maintained inward currents were observed with a —40 mV holding potential. The Ca channel antagonist nicardipine (5 μM ) blocked the transient inward current while neither of the dihydropyridine Ca channel agonists S( + )202 791 and ( — )BAY K 8644 produced a significant augmentation of sustained inward current. At 10 μM, both noradrenaline and adrenaline but not phenylephrine decreased the peak inward current. This inhibition was unaffected by a variety of adrenoceptor antagonists and was also observed when internal solutions having high Ca buffering capacity were used, but was absent when GDP-β-S instead of GTP was included in the pipette solution. The main conclusions from this study are that under our cell culture conditions, rat aortic smooth muscle cells possess predominately a transient, low-threshold-activated inward Ca current and that this Ca current is inhibited by certain adrenoceptor agonists but with a quite atypical adrenoceptor antagonist pharmacology.

scholarly journals Sustained Inward Current During Pacemaker Depolarization in Mammalian Sinoatrial Node Cells

2000 ◽  
Vol 87 (2) ◽  
pp. 88-91 ◽  
Author(s):  
Tamotsu Mitsuiye ◽  
Yasuko Shinagawa ◽  
Akinori Noma
Keyword(s):  
Sinoatrial Node ◽  
Inward Current ◽  
Sinoatrial Node Cells ◽  
Sustained Inward Current

Norepinephrine-induced sustained inward current in brown fat cells: α1-mediated by nonselective cation channels

2000 ◽  
Vol 279 (5) ◽  
pp. E963-E977 ◽  
Author(s):  
Ari Koivisto ◽  
Detlef Siemen ◽  
Jan Nedergaard
Keyword(s):  
Fold Increase ◽  
Brown Fat ◽  
Cation Channels ◽  
Current Response ◽  
Fat Cells ◽  
Adrenergic Stimulation ◽  
Open Probability ◽  
Inward Current ◽  
Nonselective Cation Channels ◽  
Sustained Inward Current

The nature of the sustained norepinephrine-induced depolarization in brown fat cells was examined by patch-clamp techniques. Norepinephrine (NE) stimulation led to a whole cell current response consisting of two phases: a first inward current, lasting for only 1 min, and a sustained inward current, lasting as long as the adrenergic stimulation was maintained. The nature of the sustained current was here investigated. It could be induced by the α1-agonist cirazoline but not by the β3-agonist CGP-12177A. Reduction of extracellular Cl− concentration had no effect, but omission of extracellular Ca2+ or Na+ totally eliminated it. When unstimulated cells were studied in the cell-attached mode, some activity of ≈30 pS nonselective cation channels was observed. NE perfusion led to a 10-fold increase in their open probability (from ≈0.002 to ≈0.017), which persisted as long as the perfusion was maintained. The activation was much stronger with the α1-agonist phenylephrine than with the β3-agonist CGP-12177A, and with the Ca2+ionophore A-23187 than with the adenylyl cyclase activator forskolin. We conclude that the sustained inward current was due to activation of ≈30 pS nonselective cation channels via α1-adrenergic receptors and that the effect may be mediated via an increase in intracellular free Ca2+ concentration.

A Ca-Induced Na-Current in Paramecium

1980 ◽  
Vol 88 (1) ◽  
pp. 305-326
Author(s):  
YOSHIRO SAIMI ◽  
CHING KUNG
Keyword(s):  
Voltage Clamp ◽  
Time Constant ◽  
Negative Resistance ◽  
Paramecium Tetraurelia ◽  
Wild Type ◽  
Na Current ◽  
Inward Current ◽  
In The Wild ◽  
Current Flows ◽  
Sustained Inward Current

Under a voltage clamp, step depolarization and repolarization can induce a sustained inward current and a tail inward current in Paramecium tetraurelia bathed in a solution containing 8 mM-Na+. These currents are best seen in the ‘paranoiac’ mutant. The I-V plot of the sustained inward current can have a region of negative resistance around −20 mV. This current is absent when Na+ is excluded from the bath solution, and it increases as the Na+ concentration increases from 2 to 8 mM. Injection of Na+ into the cell suppresses this inward current. This current develops very slowly, reaching its maximum seconds after the step depolarization and decays with a time constant of hundreds of milliseconds after the repolarization. This slow current is dependent on Ca2+. It can be suppressed by reduction or deletion of external Ca2+ or by iontophoretic injection of EGTA. ‘Pawn’ mutants with defective Caconductance also lack this current. We conclude that Paramecium has a Ca-induced conductance through which the Na-current flows. Although more prominent in the ‘paranoiac’ mutant, this Ca-induced Na-current is also seen in the wild type. This conductance may function in generating plateau depolarizations lasting seconds or even minutes and the corresponding prolonged backward swimming away from sources of irritation and stress.

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