Mechanism of inhibition of delayed rectifier K+ current by 4‐aminopyridine in rabbit coronary myocytes.

Remillard, Carmelle V.; Leblanc, Normand

doi:10.1113/jphysiol.1996.sp021223

Cited by 43 publications

(28 citation statements)

References 40 publications

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“…9B). With the exception of the reduction in g MAX, effects are consistent with a so-called reverse-use dependent block in which the blocker only attaches to the channel in the closed state and prevents transitions to the open and inactivated states (Remillard and Leblanc 1996).…”

Section: Pharmacology Of I Klsupporting

confidence: 53%

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Brichta¹,

Aubert

Eatock

et al. 2002

Journal of Neurophysiology

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Regional analysis of whole cell currents from hair cells of the turtle posterior crista. J Neurophysiol 88: 3259 -3278, 2002; 10.1152/jn.00770.2001. The turtle posterior crista is made up of two hemicristae, each consisting of a central zone containing type I and type II hair cells and a surrounding peripheral zone containing only type II hair cells and extending from the planum semilunatum to the nonsensory torus. Afferents from various regions of a hemicrista differ in their discharge properties. To see if afferent diversity is related to the basolateral currents of the hair cells innervated, we selectively harvested type I and II hair cells from the central zone and type II hair cells from two parts of the peripheral zone, one near the planum and the other near the torus. Voltage-dependent currents were studied with the whole cell, ruptured-patch method and characterized in voltage-clamp mode. We found regional differences in both outwardly and inwardly rectifying voltage-sensitive currents. As in birds and mammals, type I hair cells have a distinctive outwardly rectifying current (I K,L ), which begins activating at more hyperpolarized voltages than do the outward currents of type II hair cells. Activation of I K,L is slow and sigmoidal. Maximal outward conductances are large. Outward currents in type II cells vary in their activation kinetics. Cells with fast kinetics are associated with small conductances and with partial inactivation during 200-ms depolarizing voltage steps. Almost all type II cells in the peripheral zone and many in the central zone have fast kinetics. Some type II cells in the central zone have large outward currents with slow kinetics and little inactivation. Although these currents resemble I K,L , they can be distinguished from the latter both electrophysiologically and pharmacologically. There are two varieties of inwardly rectifying currents in type II hair cells: activation of I K1 is rapid and monoexponential, whereas that of I h is slow and sigmoidal. Many type II cells either have both inward currents or only have I K1 ; very few cells only have I h . Inward currents are less conspicuous in type I cells. Type II cells near the torus have smaller outwardly rectifying currents and larger inwardly rectifying currents than those near the planum, but the differences are too small to account for variations in discharge properties of bouton afferents innervating the two regions of the peripheral zone. The large outward conductances seen in central cells, by lowering impedances, may contribute to the low rotational gains of some central-zone afferents.

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Section: Pharmacology Of I Klsupporting

confidence: 53%

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Brichta¹,

Aubert

Eatock

et al. 2002

Journal of Neurophysiology

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“…â1.1, 1.2, 1.3 and 2.1 are present; Wang et al 1997) (Nelson & Quayle, 1995). However, the actions of 4-AP in vascular myocytes are complex and may involve closed and open channel block, as well as unblock at positive potentials (Remillard & Leblanc, 1996). For this reason, a complete characterization of the state dependence and voltage senstivity of 4-AP block of RPVKv1.5 and native KDR channels is required.…”

Section: Discussionmentioning

confidence: 99%

Identification, cloning and expression of rabbit vascular smooth muscle Kv1.5 and comparison with native delayed rectifier K⁺ current

Clément-Chomienne

Ishii

Walsh

et al. 1999

The Journal of Physiology

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Vascular smooth muscle K¤ channels play a critical role in the control of arterial tone and blood pressure by contributing to resting membrane potential and, thereby, to the regulation of L-type Ca¥ channel activation, Ca¥ influx and contraction. Several types of K¤ channels, including large conductance Ca¥-activated (BKCa), ATP-sensitive, inward rectifier, and voltage-gated, delayed rectifier (KDR) channels are believed to contribute to membrane K¤ conductance depending on the vascular bed, physiological condition and presence of vasoactive agonists (Nelson & Quayle, 1995). Rapidly activating and slowly inactivating KDR channels have been the focus of several recent studies and it is now recognized that these channels participate in (i) control of myogenic tone in resistance vasculature (Knot & Nelson, 1995), (ii) the vasodilatory and constrictor responses of some vessels to vasoactive agonists (Satake et al. 1996;Dong et al. 1998), and (iii) the response of vascular myocytes to the activation of serineÏthreonine kinases, e.g. cAMPdependent protein kinase (PKA) and protein kinase C (PKC) (

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“…The experimental effects of NFA were simulated mathematically using a computer-modeling method similar to that reported previously by our group (Remillard and Leblanc, 1996). Figure 7 displays the various kinetic schemes that were tested.…”

Section: Under Kmentioning

confidence: 99%

Dynamics of Ca²⁺-Dependent Cl^- Channel Modulation by Niflumic Acid in Rabbit Coronary Arterial Myocytes

Ledoux

Greenwood²,

Leblanc³

2004

Mol Pharmacol

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Calcium-activated chloride channels (Cl Ca ) are crucial regulators of vascular tone by promoting a depolarizing influence on the resting membrane potential of vascular smooth muscle cells. Niflumic acid (NFA), a potent blocker of Cl Ca in vascular myocytes, was shown recently to cause inhibition and paradoxical stimulation of sustained calcium-activated chloride currents [I Cl(Ca) ] in rabbit pulmonary artery myocytes. The aims of the present study were to investigate whether NFA produced a similar dual effect in coronary artery smooth muscle cells and to determine the concentration-dependence and dynamics of such a phenomenon. Sustained I Cl(Ca) evoked by intracellular Ca 2ϩ clamped at 500 nM were dose-dependently inhibited by NFA (IC 50 ϭ 159 M) and transiently augmented in a concentration-independent manner (10 M to 1 mM) ϳ2-fold after NFA removal. However, the time to peak and duration of NFAenhanced I Cl(Ca) increased in a concentration-dependent fashion. Moreover, the rate of recovery was reduced by membrane depolarization, suggesting the involvement of a voltage-dependent step in the interaction of NFA, leading to stimulation of

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Mechanism of inhibition of delayed rectifier K+ current by 4‐aminopyridine in rabbit coronary myocytes.

Abstract: shifting the activation curve of these channels to more positive potentials.

Cited by 43 publications

References 40 publications

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Identification, cloning and expression of rabbit vascular smooth muscle Kv1.5 and comparison with native delayed rectifier K⁺ current

Dynamics of Ca²⁺-Dependent Cl^- Channel Modulation by Niflumic Acid in Rabbit Coronary Arterial Myocytes

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Mechanism of inhibition of delayed rectifier K+ current by 4‐aminopyridine in rabbit coronary myocytes.

Abstract: shifting the activation curve of these channels to more positive potentials.

Cited by 43 publications

References 40 publications

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Regional Analysis of Whole Cell Currents From Hair Cells of the Turtle Posterior Crista

Identification, cloning and expression of rabbit vascular smooth muscle Kv1.5 and comparison with native delayed rectifier K+ current

Dynamics of Ca2+-Dependent Cl- Channel Modulation by Niflumic Acid in Rabbit Coronary Arterial Myocytes

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Product

Resources

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Identification, cloning and expression of rabbit vascular smooth muscle Kv1.5 and comparison with native delayed rectifier K⁺ current

Dynamics of Ca²⁺-Dependent Cl^- Channel Modulation by Niflumic Acid in Rabbit Coronary Arterial Myocytes