Block of large conductance Ca(2+)‐activated K+ channels in rabbit vascular myocytes by internal Mg2+ and Na+.

Salinas, Elizabeth Morales; Cole, W. C.; Remillard, Carmelle V.; Leblane, N

doi:10.1113/jphysiol.1996.sp021627

Cited by 43 publications

(43 citation statements)

References 40 publications

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“…In cell-attached patches BK channel conductance was smaller than that recorded following excision of the patch. This observation has been already documented for BK channels in other smooth muscle tissues [28,44], and interpreted to be due to voltage-dependent block of the BK channel by intracellular Mg and Na ions, and polyamines. This behaviour is illustrated in Fig.…”

Section: Single Bk Channel Recordings From Intact Myocytesmentioning

confidence: 55%

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Catacuzzeno

Pisconti

Harper

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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We used the patch-clamp method to characterize the BK channel in freshly isolated myocytes from the saphenous branch of the rat femoral artery. Single-channel recordings revealed that the BK channel had a conductance of 187 pS in symmetrical 150 mM KCl, was blocked by external tetraethylammonium (TEA) with a KD(TEA) of approx. 300 microM at +40 mV, and by submicromolar charybdotoxin (CTX). The sensitivity of the BK channel to Ca was especially high (KD(ca) approx. 0.1 microM at +60 mV) compared to skeletal muscle and neuronal tissues. We also investigated the macroscopic K current, which under certain conditions is essentially sustained by BK channels. This conclusion is based on the findings that the macroscopic current activated upon depolarization follows a single exponential time course and is virtually fully blocked by 100 nM CTX and 5 mM external TEA. We made use of this occurrence to assess the voltage and Ca dependence of the macroscopic BK current. In intact myocytes, the BK channel showed a strong and voltage-dependent reduction of the outward current (62% at +40 mV), most likely due to block by intracellular Ba and polyamines. The results obtained from macroscopic and unitary current indicate that approx. 2.5% of the BK channels are active under physiological conditions, sustaining approx. 20 pA of outward current. Given the high input resistance of these cells, few BK channels are required to open in order to cause a significant membrane hyperpolarization, and thus function to limit the contraction resulting from acute increases in intravascular pressure, or in response to hypertensive pathologies.

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Section: Single Bk Channel Recordings From Intact Myocytesmentioning

confidence: 55%

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Catacuzzeno

Pisconti

Harper

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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“…3A) compared with those in insideout recordings might be due to higher cytoplasmic Mg¥ or Na¤ ion concentrations in the neurones, which reduce the amplitudes, especially at potentials positive to 0 mV (Morales et al 1996). Most previous studies described the BKCa current as a slow one, which needed up to some hundreds of milliseconds for full activation, but in order to obtain fast activation, 40-100 ìmol l¢ Ca¥ at the cytoplasmic membrane side was necessary (Egan et al 1993;Gola & Crest, 1993;Morales et al 1996). Since in neuronal cells BKCa channels are said to contribute to the action potential, it is evident that they should activate quickly at depolarizing potentials.…”

Section: Single-channel Kineticsmentioning

confidence: 96%

Properties and functions of calcium‐activated K⁺ channels in small neurones of rat dorsal root ganglion studied in a thin slice preparation

Scholz

Gruß

Vogel

1998

The Journal of Physiology

100

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Properties, kinetics and functions of large conductance calcium‐activated K+ channels (BKCa) were investigated by the patch‐clamp technique in small neurones (Aδ‐ and C‐type) of a dorsal root ganglion (DRG) thin slice preparation without enzymatic treatment. Unitary conductance of BKCa channels measured in symmetrical high K+ solutions (155 mm) was 200 pS for inward currents, and chord conductance in control solution was 72 pS. Potentials of half‐maximum activation (V1/2) of the channels were linearly shifted by 43 mV per log10[Ca2+]i unit (pCa) in the range of −28 mV (pCa 4) to +100 mV (pCa 7). Open probabilities increased e‐times per 15–32 mV depolarization of potential. In mean open probability, fast changes with time were mainly observed at pCa > 6 and at potentials > +20 mV, without obvious changes in the experimental conditions. BKCa channels were half‐maximally blocked by 0.4 mm TEA, measured by apparent amplitude reductions. They were completely blocked by 100 nm charybdotoxin and 50 nm iberiotoxin by reduction of open probability. Two subtypes of small DRG neurones could be distinguished by the presence (type I) or absence (type II) of BKCa channels. In addition, less than 10 % of small neurones showed fast (∼135 V s−1) and short (∼0.8 ms) action potentials (AP). The main functions of BKCa channels were found to be shortening of AP duration, increasing of the speed of repolarization and contribution to the fast after‐hyperpolarization. As a consequence, BKCa channels may reduce the amount of calcium entering a neurone during an AP. BKCa channel currents suppressed a subsequent AP and prolonged the refractory period, which might lead to a reduced repetitive activity. We suggest that the BKCa current is a possible mechanism of the reported conduction failure during repetitive stimulation in DRG neurones.

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“…5B) (Morales, Cole, Remillard & Leblanc, 1996), in pancreatic beta cells (Tabcharani & Misler, 1989), and in chromaffin cells (Yellen, 1984). Na+ was known to block voltage dependently other K+ channels, such as the inward rectifier K+ channel (Harvey & Ten Eick, 1989) and the channel for A current (Forsythe, Linsdell & Stanfield, 1992).…”

Section: Effects Of Adenosine Adp and Atpmentioning

confidence: 99%

“…Na+ was known to block voltage dependently other K+ channels, such as the inward rectifier K+ channel (Harvey & Ten Eick, 1989) and the channel for A current (Forsythe, Linsdell & Stanfield, 1992). In addition, other monovalent cations, such as Cs', are known to have similar effects on K+ channels (Fukushima, 1982;Tabcharani & Misler, 1989 (Morales et al 1996) and pulmonary arteries (Snetkov, Gurney, Ward & Osipenko, 1996). …”

Section: Effects Of Adenosine Adp and Atpmentioning

confidence: 99%

Effects of intracellular N+, M2+ and metabolites on C2+−activated K+ channels in pulmonary and ear arterial smooth muscle cells of the rabbit

Lee

Earm

1998

Experimental Physiology

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SUMMARYHypoxic pulmonary vasoconstriction (HPV) is an important mechanism for matching the ventilation/perfusion ratio in the lung, but the signal transduction pathway through which hypoxia induces vasoconstriction remains unclear. We hypothesized that the decrease in K+ current induced by hypoxia is a key mechanism for HPV, and examined the effects of the substances which are expected to accumulate during hypoxia on the activity of large conductance Ca2+-activated K+ (BKCa) channels. Pulmonary and ear arterial smooth muscle cells were isolated from the rabbit using enzymatic digestion, and large conductance Ca2+-activated K+ current (IBK,Ca) was recorded in symmetrical K+ concentrations using the inside-out mode of the patch-clamp technique. Increasing the Na+ concentration on the intracellular side suppressed IBK,Ca dose dependently: 4.6, 20.9, 35-5 and 44.6 % reduction with 4, 8, 12 and 16 mM Na+, respectively. Mg2' also reduced IBK,Ca' and the maximum reduction was obtained at 0 5 mM. Lactate, adenosine, ADP and ATP did not significantly affect IBK,Ca. There was no difference between pulmonary and ear arterial smooth muscle cells in their response to the above substances; this finding rules out modulation of BKCa channels by the various factors thought to accumulate during hypoxia as a major mechanism involved in the decrease in the K+ conductance of pulmonary arteries in hypoxia.

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Block of large conductance Ca(2+)‐activated K+ channels in rabbit vascular myocytes by internal Mg2+ and Na+.

Cited by 43 publications

References 40 publications

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Properties and functions of calcium‐activated K⁺ channels in small neurones of rat dorsal root ganglion studied in a thin slice preparation

Effects of intracellular N+, M2+ and metabolites on C2+−activated K+ channels in pulmonary and ear arterial smooth muscle cells of the rabbit

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Block of large conductance Ca(2+)‐activated K+ channels in rabbit vascular myocytes by internal Mg2+ and Na+.

Cited by 43 publications

References 40 publications

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Characterization of the large-conductance Ca-activated K channel in myocytes of rat saphenous artery

Properties and functions of calcium‐activated K+ channels in small neurones of rat dorsal root ganglion studied in a thin slice preparation

Effects of intracellular N+, M2+ and metabolites on C2+−activated K+ channels in pulmonary and ear arterial smooth muscle cells of the rabbit

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Properties and functions of calcium‐activated K⁺ channels in small neurones of rat dorsal root ganglion studied in a thin slice preparation