Activation of squid axon K+ channels. Ionic and gating current studies.

White, Michael M.; Bezanilla, Francisco

doi:10.1085/jgp.85.4.539

Cited by 95 publications

(105 citation statements)

References 25 publications

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“…It follows that this step is likely to be the most voltage dependent, since depolarization must very substantially increase the transition rate of that step. White & Bezanilla (1985) have argued from their measurements of potassium channel gating current in squid axon that, since it contributes negligible gating current, the first step in activation of potassium channels is either the slowest or the least voltage dependent. Our own measurements of bursting behaviour in Rb+ suggest that, though it may well be the slowest step, an early step in activation is more voltage dependent than later ones.…”

Section: Discussionmentioning

confidence: 99%

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Spruce

Standen

Stanfield

1989

The Journal of Physiology

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SUMMARY1. Unitary currents were measured through delayed rectifier potassium channels of frog skeletal muscle, under conditions where either potassium or rubidium ions carried current.2. Unitary currents were reduced in amplitude when Rb+ was the charge carrier, indicating that Rb+ permeated the channel less readily than did K+. On the other hand permeability ratios (PRb/PK) measured from the change in reversal potential upon ionic substitution were 092 for the external and 067 for the internal mouth of the channel.3. 5. The prolongation in Rb+ of tail currents under repolarization was associated with increases in the number of openings per burst and in the number of bursts during each tail.6. The implications of these results for channel gating are discussed. It is argued that an early step in channel activation is more voltage dependent than later steps.

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Section: Discussionmentioning

confidence: 99%

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Spruce

Standen

Stanfield

1989

The Journal of Physiology

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“…(see Hille, 1984). With regard to a general sequential activation scheme White & Bezanilla (1985) pointed out that, in doublepulse experiments similar to the ones used here, the time required for activation at the second pulse will be shorter if the last step (i.e. the closed-open transition) is not rate limiting.…”

Section: Models For the Kinetic Behaviour Of The Channelsmentioning

confidence: 96%

Fast gating kinetics of the slow Ca2+ current in cut skeletal muscle fibres of the frog.

Feldmeyer

Melzer

Pohl

et al. 1990

The Journal of Physiology

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SUMMARY1. Calcium currents and intramembrane charge movements were measured in cut twitch muscle fibres of the frog and the time course of activation of the current was studied using various conditioning pulse protocols.2. When a conditioning activation was produced by a depolarizing pulse which ended before inactivation occurred, a subsequent depolarization led to a faster onset of activation, indicating that the system had not completely returned to the initial state during the interval between the two pulses.3. The interval between conditioning and test pulse was varied at different subthreshold potentials to study the time course of restoring the steady-state conditions. Complete restoration required a waiting period of about 1 min at the holding potential of -80 mV due to a very slow process but partial recovery was reached within 100 ms. This initial recovery process was strongly voltage dependent and became considerably slower when the interval potential approached the threshold for current activation.4. Stepping to a roughly 10 mV subthreshold potential without applying a conditioning activation caused no change in the time course of the current produced by a subsequent test depolarization. Depolarizing just to the current threshold caused a slowly progressing acceleration of test current activation.5. The peak current-voltage relation in the fast gating regime caused by a conditioning activation coincided with the current-voltage relation measured under steady-state conditions, indicating not that a new channel population had become activated but that the same channels showed a different gating behaviour.6. Intramembrane charge movements measured in 2 mM-Cd2+ and tested at potentials between -40 and + 40 mV showed negligible changes when preceded by a strong depolarization. 7. We discuss several possible models which can explain the fact that the current is speeded up by a conditioning activation while the charge movements remain unchanged. It is possible that the fast voltage-dependent transition which becomes visible after conditioning pulses reflects a rapid conformational change of the Ca2+ channel molecule which also occurs during its normal gating mode but remains undetectable in terms of conductance. In view of the hypothesis that the Ca2+ channel molecule forms a voltage sensor for excitation-contraction coupling this fast MS 7918 348

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“…The activation kinetics were determined by fitting a single exponential to the latter 50% of activation. 26 The curve-fitting procedure used a nonlinear least squares (Gauss-Newton) algorithm, and goodness of fit was judged by the 2 criterion.…”

Section: Pulse Protocols and Analysismentioning

confidence: 99%

Oxygen Sensitivity of Cloned Voltage-Gated K ⁺ Channels Expressed in the Pulmonary Vasculature

Hulme

Coppock

Felipe

et al. 1999

Circulation Research

155

161

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Abstract-Hypoxic pulmonary vasoconstriction is initiated by inhibiting one or more voltage-gated potassium (Kv) channel in the vascular smooth muscle cells (VSMCs) of the small pulmonary resistance vessels. Although progress has been made in identifying which Kv channel proteins are expressed in pulmonary arterial (PA) VSMCs, there are conflicting reports regarding which channels contribute to the native O 2 -sensitive K ϩ current. In this study, we examined the effects of hypoxia on the Kv1.2, Kv1.5, Kv2.1, and Kv9.3 ␣ subunits expressed in mouse L cells using the whole-cell patch-clamp technique. Hypoxia (PO 2 ϭϷ30 mm Hg) reversibly inhibited Kv1.2 and Kv2.1 currents only at potentials more positive than 30 mV. In contrast, hypoxia did not alter Kv1.5 current. Currents generated by coexpression of Kv2.1 with Kv9.3 ␣ subunits were reversibly inhibited by hypoxia in the voltage range of the resting membrane potential (E M ) of PA VSMCs (Ϸ28% at Ϫ40 mV). Coexpression of Kv1.2 and Kv1.5 ␣ subunits produced currents that displayed kinetic and pharmacological properties distinct from Kv1.2 and Kv1.5 channels expressed alone. Moreover, hypoxia reversibly inhibited Kv1.2/Kv1.5 current activated at physiologically relevant membrane potentials (Ϸ65% at Ϫ40 mV). These results indicate that (1) hypoxia reversibly inhibits Kv1.2 and Kv2.1 but not Kv1.5 homomeric channels, (2) Kv1.2 and 1.5 ␣ subunits can assemble to form an O 2 -sensitive heteromeric channel, and (3) Key Words: Kv channel Ⅲ hypoxia Ⅲ pulmonary artery Ⅲ heteromeric H ypoxia induces constriction of the small pulmonary resistance arteries, a process known as hypoxic pulmonary vasoconstriction (HPV). 1 This constrictor response is the opposite of that which occurs in resistance vessels of the systemic circulation. In these vessels, hypoxia results in vasodilation. 2 In the fetus, HPV contributes to high pulmonary arterial resistance by diverting blood flow through the ductus arteriosus. 3 In the adult, HPV reduces blood flow through atelectatic or underventilated areas of the lung where ventilation is not adequate for oxygenation. 3 In this way, short-term HPV is an essential mechanism that helps match ventilation to perfusion, diverting blood flow away from poorly ventilated regions of the lung to maximize arterial saturation. 4 However, when hypoxia becomes more generalized, as seen in patients suffering from either long-term obstructive lung diseases or high altitude exposure, 4,5 the subsequent pulmonary vasoconstriction causes an increase in pulmonary arterial pressure that can lead to the development of pulmonary hypertension.In pulmonary arterial (PA) vascular smooth muscle cells (VSMCs), voltage-gated potassium (Kv) channels play an important role in setting the resting membrane potential (E M ϭϷϪ55 mV) and, consequently, vascular tone. 6 -8 It is thought that hypoxia reversibly inhibits Kv channels and, thereby, regulates vasoconstriction. 7,9 -12 This hypothesis is supported by the observation that hypoxia inhibits whole-cell K ϩ currents and ca...

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Activation of squid axon K+ channels. Ionic and gating current studies.

Cited by 95 publications

References 25 publications

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Fast gating kinetics of the slow Ca2+ current in cut skeletal muscle fibres of the frog.

Oxygen Sensitivity of Cloned Voltage-Gated K ⁺ Channels Expressed in the Pulmonary Vasculature

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Activation of squid axon K+ channels. Ionic and gating current studies.

Cited by 95 publications

References 25 publications

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Rubidium ions and the gating of delayed rectifier potassium channels of frog skeletal muscle.

Fast gating kinetics of the slow Ca2+ current in cut skeletal muscle fibres of the frog.

Oxygen Sensitivity of Cloned Voltage-Gated K + Channels Expressed in the Pulmonary Vasculature

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Oxygen Sensitivity of Cloned Voltage-Gated K ⁺ Channels Expressed in the Pulmonary Vasculature