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Digitale Medien

Activation of Inwardly Rectifying Potassium Channels by Muscarinic Receptor-linked G Protein in Isolated Human Ventricular Myocytes (1997)

Koumi, S-i. ; Sato, R. ; Nagasawa, K. ; [weitere]

Springer

The journal of membrane biology 157 (1997), S. 71 -81

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ISSN: 1432-1424

Schlagwort(e): Key words: Patch-clamp technique — Human ventricular myocytes — G proteins — Muscarinic K+ channel — Inwardly-rectifying K+ channel

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie

Notizen: Abstract. Muscarinic receptor-linked G protein, G i , can directely activate the specific K+ channel (I K(ACh)) in the atrium and in pacemaker tissues in the heart. Coupling of G i to the K+ channel in the ventricle has not been well defined. G protein regulation of K+ channels in isolated human ventricular myocytes was examined using the patch-clamp technique. Bath application of 1 μm acetylcholine (ACh) reversibly shortened the action potential duration to 74.4 ± 12.1% of control (at 90% repolarization, mean ±sd, n= 8) and increased the whole-cell membrane current conductance without prior β-adrenergic stimulation in human ventricular myocytes. The ACh effect was reversed by atropine (1 μm). In excised inside-out patch configurations, application of GTPγS (100 μm) to the bath solution (internal surface) caused activation of I K(ACh) and/or the background inwardly-rectifying K+ channel (I K1) in ventricular cell membranes. I K(ACh) exhibited rapid gating behavior with a slope conductance of 44 ± 2 pS (n= 25) and a mean open lifetime of 1.8 ± 0.3 msec (n= 21). Single channel activity of GTPγS-activated I K1 demonstrated long-lasting bursts with a slope conductance of 30 ± 2 pS (n= 16) and a mean open lifetime of 36.4 ± 4.1 msec (n= 12). Unlike I K(ACh), G protein-activated I K1 did not require GTP to maintain channel activity, suggesting that these two channels may be controlled by G proteins with different underlying mechanisms. The concentration of GTP at half-maximal channel activation was 0.22 μm in I K(ACh) and 1.2 μm in I K1. Myocytes pretreated with pertussis toxin (PTX) prevented GTP from activating these channels, indicating that muscarinic receptor-linked PTX-sensitive G protein, G i , is essential for activation of both channels. G protein-activated channel characteristics from patients with terminal heart failure did not differ from those without heart failure or guinea pig. These results suggest that ACh can shorten the action potential by activating I K(ACh) and I K1 via muscarinic receptor-linked G i proteins in human ventricular myocytes.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/s002329900217

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Digitale Medien

Characterization of the acetylcholine-sensitive muscarinic K+ channel in isolated feline atrial and ventricular myocytes (1995)

Koumi, S -i. ; Sato, R. ; Hayakawa, H.

Springer

The journal of membrane biology 145 (1995), S. 143-150

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ISSN: 1432-1424

Schlagwort(e): Patch clamp technique ; Acetylcholine ; Muscarinic K+ channel ; GTP — G protein

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie

Notizen: Abstract M2-cholinergic receptor activation by acetylcholine (ACh) is known to cause a negative inotropic and chronotropic action in atrial tissues. This effect is still controversial in ventricular tissues. The ACh-sensitive muscarinic K+ channel (I K(ACh)) activity was characterized in isolated feline atrial and ventricular myocytes using the patch-clamp technique. Bath application of ACh (1 μm) caused shortening of action potential duration without prior stimulation with catecholamines in atrial and ventricular myocytes. Resting membrane potential was slightly hyperpolarized in both tissues. These effects of ACh were greater in atrium than in ventricle. ACh increased whole-cell membrane current in atrial and ventricular myocytes. The current-voltage (I-V) relationship of the ACh-induced current in ventricle exhibited inward-rectification whose slope conductance was smaller than that in atrium. In single channel recording from cell-attached patches, I K(ACh) activity was observed when ACh was induced in the pipette solution in both tissues. The channel exhibited a slope conductance of 47 ±1 pS (mean ± sd, n=14) in atrium and 47 ±2 pS (n= 10) in ventricle (not different statistically; ns). The open times were distributed according to a single exponential function with mean open lifetime of 2.0±0.3 msec (n= 14) in atrium and 1.9±0.3 msec (n=10) in ventricle (ns); these conductance and kinetic properties were similar between the two tissues. However, the relationship between the concentration of ACh and single channel activity showed a higher sensitivity to ACh in atrium (IC 50 =0.03 μm) than in ventricle (IC 50 =0.15 μm). In excised inside-out patches, ventricular I K(ACh) required higher concentrations of GTP to activate the channel compared to atrial channels. These results suggest a reduced I K(ACh) channel sensitivity to M2-cholinergic receptor-linked G protein (Gi) in ventricle compared to atrium in feline heart.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00237372

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Digitale Medien

Modulation of the inwardly rectifying K+ channel in isolated human atrial myocytes by α1-adrenergic stimulation (1995)

Sato, R. ; Koumi, S-i.

Springer

The journal of membrane biology 148 (1995), S. 185-191

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ISSN: 1432-1424

Schlagwort(e): Inwardly rectifying K+ channel ; Patch ; clamp technique ; Human atrial myocytes ; Methox ; amine ; Protein kinase C

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie

Notizen: Abstract We have examined the α1-adrenergic modulation of the inwardly-rectifying K+ channel (I K1) in isolated human atrial myocytes using the patch clamp technique. α1-Adrenergic agonist methoxamine produced action potential prolongation and a depolarization of the resting membrane potential. Under whole-cell voltage clamp conditions, bath application of methoxamine can inhibit macroscopic I K1. The methoxamine-induced inhibition was reversible and concentration dependent, with the concentration for half-maximal inhibition being 18 μm. The methoxamine-induced inhibition of I K1 was prevented by bath application of α1-adrenergic blocker prazosin. The current was similarly inhibited by phorbol ester (PMA), an activator of protein kinase C (PKC). In contrast, methoxamine failed to inhibit the current in the presence of a specific PKC inhibitor H-9, suggesting that PKC is involved in the methoxamine-induced inhibition of I K1. In single channel recording from cell attached patches, bath-applied methoxamine could suppress I K1 channels by decreasing the frequency and duration of bursting without affecting unitary amplitude. Direct application of purified PKC to excised inside-out patches inhibited channel activity similar to methoxamine in cell-attached patches. The PKC selective inhibitor, PKC19-36, prevented the PKC-induced inhibition of the channel. We conclude that human atrial I K1 can be inhibited by α1-adrenergic stimulation via PKC-dependent pathways.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00207274

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Characterization of the Stretch-activated Chloride Channel in Isolated Human Atrial Myocytes (1998)

Sato, R. ; Koumi, S-i.

Springer

The journal of membrane biology 163 (1998), S. 67-76

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ISSN: 1432-1424

Schlagwort(e): Key words: Patch-clamp technique — Stretch-activated Cl− channel — Human atrial myocytes

Quelle: Springer Online Journal Archives 1860-2000

Thema: Biologie , Chemie und Pharmazie

Notizen: Abstract: Macroscopic and unitary currents through stretch-activated Cl− channels were examined in isolated human atrial myocytes using whole-cell, excised outside-out and inside-out configurations of the patch-clamp technique. When K+ and Ca2+ conductances were blocked and the intracellular Ca2+ concentration ([Ca2+] i ) was reduced, application of positive pressure via the pipette activated membrane currents under whole-cell voltage-clamp conditions. The reversal potential of the current shifted by 60 mV per 10-fold change in the external Cl− concentration, indicating that the current was Cl− selective. The current was inhibited by bath application of 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) and 9-anthracenecarboxylic acid (9-AC). β-Adrenergic stimulation failed to activate a Cl− current. In single channel recordings from outside-out patches, positive pressure in the pipette activated the unitary current with half-maximal activation of 14.7 mm Hg at +40 mV. The current-voltage relationship of single channel activity obtained in inside-out patches was linear in symmetrical Cl− solution with the averaged slope conductance of 8.6 ± 0.7 pS (mean ±sd, n= 10). The reversal potential shift of the channel by changing Cl− concentration was consistent with a Cl− selective channel. The open time distribution was best described by a single exponential function with mean open lifetime of 80.4 ± 9.6 msec (n= 9), while at least two exponentials were required to fit the closed time distributions with a time constant for the fast component of 11.5 ± 2.2 msec (n= 9) and that for the slow component of 170.2 ± 21.8 msec (n= 9). Major changes in the single channel activity in response to pressure were caused by changes in the interburst interval. Single channel activity was inhibited by DIDS and 9-AC in a manner similar to whole-cell configuration. These results suggest that membrane stretch induced by applying pressure via the pipette activated a Cl− current in human atrial myocytes. The current was sensitive to Cl− channel blockers and exhibited membrane voltage-independent bursting opening without sensitive to β-adrenergic stimulation.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/s002329900371

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A new adhesion process of glass to metal using the redox reaction (1996)

Seki, H. ; Satoh, K. ; Satoh, H. ; [weitere]

Springer

Journal of materials science 31 (1996), S. 4891-4898

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ISSN: 1573-4803

Quelle: Springer Online Journal Archives 1860-2000

Thema: Maschinenbau

Notizen: Abstract A new adhesion process of glass to metal was developed based on the redox reaction without oxidation of the metal surface. PbO-based glasses were strongly adhered to nickel metal at low temperature (400–500 °C) in a low-oxygen atmosphere (〈 0.1 p.p.m.). The interfaces between glasses and metal were analysed by SEM-EDS. It was found that the reaction layer and lead metal were formed by the redox reaction at the interface. In the case of the adhesion of PbO-based glasses containing CuO to nickel, the main reduced product in the glass was Cu2O, and lead was not detected. The redox reaction was simulated by a thermodynamic equilibrium theory; the results agreed with the analysis by SEM-EDS.

Materialart: Digitale Medien

URL: http://dx.doi.org/10.1007/BF00355877

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