scholarly journals Two functionally distinct 4-aminopyridine-sensitive outward K+ currents in rat atrial myocytes.

1992 ◽  
Vol 100 (6) ◽  
pp. 1041-1067 ◽  
Author(s):  
W A Boyle ◽  
J M Nerbonne
Keyword(s):  
Experimental Testing ◽  
Potential Range ◽  
Kinetic Properties ◽  
Atrial Myocytes ◽  
Adult Rat ◽  
Outward Currents ◽  
Recovery From Inactivation ◽  
Functional Inactivation ◽  
The Individual ◽  
K Currents

In the experiments here, the detailed kinetic properties of the Ca(2+)-independent, depolarization-activated outward currents (Iout) in enzymatically dispersed adult rat atrial myocytes were studied. Although there is only slight attenuation of peak Iout during brief (100 ms) voltage steps, substantial decay is evident during long (10 s) depolarizations. The analyses here reveal that current inactivation is best described by the sum of two exponential components, which we have termed IKf and IKs to denote the fast and slow components, respectively, of Iout decay. At all test potentials, IKf inactivates approximately 20-fold more rapidly than IKs. Neither the decay time constants nor the fraction of Iout remaining at the end of 10-s depolarizations varies over the potential range of 0 to +50 mV, indicating that the rates of inactivation and recovery from inactivation are voltage independent. IKf recovers from inactivation completely, independent of the recovery of IKs, and IKf recovers approximately 20 times faster than IKs. The pharmacological properties of IKf and IKs are similar: both components are sensitive to 4-aminopyridine (1-5 mM) and both are relatively resistant to externally applied tetraethylammonium (50 mM). Taken together, these findings suggest that IKf and IKs correspond to two functionally distinct K+ currents with similar voltage-dependent properties and pharmacologic sensitivities, but with markedly different rates of inactivation and recovery from inactivation. From the experimental data, several gating models were developed in which voltage-independent inactivation is coupled either to channel opening or to the activation of the individual channel subunits. Experimental testing of predictions of these models suggests that voltage-independent inactivation is coupled to activation, and that inactivation of only a single subunit is required to result in functional inactivation of the channels. This model closely approximates the properties of IKf and IKs, as well as the composite outward currents, measured in adult rat atrial myocytes.

Phenylephrine suppresses outward K+ currents in rat atrial myocytes

1996 ◽  
Vol 271 (3) ◽  
pp. H937-H946 ◽  
Author(s):  
D. R. Van Wagoner ◽  
M. Kirian ◽  
M. Lamorgese
Keyword(s):  
Current Component ◽  
Atrial Myocytes ◽  
Adrenergic Agonist ◽  
Whole Cell ◽  
K Channels ◽  
Recovery From Inactivation ◽  
Cell Recording ◽  
K Current ◽  
Kinetics Of ◽  
K Currents

The modulation of whole cell K+ currents by the alpha 1-adrenergic agonist, phenylephrine, was studied in isolated rat atrial myocytes by use of perforated-patch whole cell recording techniques. The out ward K+ current in these myocytes consists of two inactivating components (iK,f and iK,s), which differ in the kinetics of inactivation and recovery from inactivation, and a noninactivating component, (iK,ss). Superfusion of these myocytes with 10 microM phenylephrine caused a rapid suppression of iK,ss, with little effect on the other current components. This effect of phenylephrine could be mimicked by exogenous application of 1,2-dioctanoyl-sn-glycerol (20 microM), a membrane-permeant diacylglycerol analogue; however, it was clearly distinct from the effect of 5 nM alpha-dendrotoxin, which selectively suppressed the slowly inactivating current component, iK,s, while having no effect on iK,ss. At a dose of 50 microM, phenylephrine also suppressed iK,s. There was no significant effect of phenylephrine (10 or 50 microM) or alpha-dendrotoxin (5 nM) on the rapidly inactivating current component, iK,f. The kinetic and pharmacological differences between these current components suggest that they represent the activity of distinct K+ channels.

A novel type of depolarization-activated K+ current in isolated adult rat atrial myocytes

1991 ◽  
Vol 260 (4) ◽  
pp. H1236-H1247 ◽  
Author(s):  
W. A. Boyle ◽  
J. M. Nerbonne
Keyword(s):  
Ventricular Myocytes ◽  
Outward Current ◽  
Cdna Libraries ◽  
K Channel ◽  
Delayed Rectifier ◽  
Atrial Myocytes ◽  
Patch Clamp Recording ◽  
K Channels ◽  
Adult Rat ◽  
K Currents

To determine the types of voltage-gated K+ channels controlling action potential repolarization in atrial cells, we have characterized the properties of depolarization-activated K+ channels in isolated adult rat atrial myocytes using the whole cell patch-clamp recording technique. On membrane depolarization, Ca2(+)-independent outward K+ currents in these cells begin to activate at approximately -40mV. At all test potentials, the currents activate rapidly after a delay, and there is little or no decay of the peak outward current amplitude during brief (100 ms) depolarizations. In addition, the currents show little steady-state inactivation at membrane potentials negative to -60 mV. The currents are blocked effectively by 1-5 mM 4-aminopyridine but are relatively insensitive to extracellular tetraethylammonium at concentrations up to 50 mM. Based on the measured time- and voltage-dependent properties and the pharmacological sensitivity of the currents, we suggest that the depolarization-activated K+ channels underlying the macroscopic currents in adult rat atrial myocytes are distinct from those described previously in other myocardial preparations, including adult rat ventricular myocytes. Interestingly, the outward K+ currents characterized here in isolated adult rat atrial myocytes are remarkably similar to those of several recently described "delayed rectifier" K+ channel genes isolated from rat brain cDNA libraries and expressed in Xenopus oocytes, suggesting that similar K+ currents are likely present in cells of the mammalian central nervous system.

Na+, K+ and Ca2+ currents in identified leech neurones in culture

1989 ◽  
Vol 141 (1) ◽  
pp. 1-20
Author(s):  
R. R. Stewart ◽  
J. G. Nicholls ◽  
W. B. Adams
Keyword(s):  
Minor Component ◽  
Outward Current ◽  
Membrane Properties ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Channel Blockers ◽  
Sensory Neurones ◽  
K Current ◽  
The Individual ◽  
K Currents

1. Na+, K+ and Ca2+ currents have been measured by voltage-clamp in Retzius (R), anterior pagoda (AP) and sensory (pressure, touch and nociceptive) cells dissected from the central nervous system (CNS) of the leech. These cells maintain their distinctive membrane properties and action potential configurations in culture. Currents carried by the individual ions were analysed by the use of channel blockers and by their kinetics. Since the cells are isopotential they can be voltage-clamped effectively. 2. Depolarization, as expected, gave rise to an early inward Na+ current followed by a delayed outward K+ current. In Na+-free medium containing tetraethylammonium (TEA+), and in the presence of 4-aminopyridine (4-AP), inward Ca2+ currents were revealed that inactivated slowly and were blocked by Cd2+ and Mn2+. 3. Na+ and Ca2+ currents were similar in their characteristics in R. AP and sensory neurones. In contrast, K+ currents showed marked differences. Three principal K+ currents were identified. These differed in their time courses of activation and inactivation and in their responses to Ca2+ channel blockers. 4. K+ currents of the A-type (IA) activated and inactivated rapidly, were not affected by Ca2+ channel blockers and were eliminated by steady-state inactivation at holding potentials of −30 mV. A-type K+ currents were found in AP cells and as a minor component of the outward current in R cells. A Ca2+-activated K+ current (IC), that inactivated more slowly and was reduced by Ca2+ channel blockers, constituted the major outward current in R cells. The third K+ current resembled the delayed rectifier currents (IK1 and IK2) of squid axons with slow activation and inactivation kinetics. Such currents were found in R cells and in the sensory neurones (T, P and N). 5. The principal differences in membrane properties of identified leech neurones can be explained in terms of the numbers of Na+ channels and the distinctive kinetics of K+ channels in each type of cell.

Temperature-dependence of L-type Ca(2+) channel current in atrial myocytes from rainbow trout

2000 ◽  
Vol 203 (18) ◽  
pp. 2771-2780 ◽  
Author(s):  
H.A. Shiels ◽  
M. Vornanen ◽  
A.P. Farrell
Keyword(s):  
Rainbow Trout ◽  
Temperature Dependence ◽  
Voltage Clamp ◽  
Pulse Voltage ◽  
Kinetic Properties ◽  
Temperature Dependency ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Channel Current ◽  
Series Of Experiments

Rainbow trout, Oncorhynchus mykiss, inhabit eurythermal environments and must therefore be able to cope with changes in environmental temperature. As ectotherms, their heart is required to maintain cardiac function over a range of ambient water temperatures. This raises important questions concerning the temperature-dependence of cardiac ion channel function in fish hearts, in particular, the channels involved in Ca(2+) transport. Thus, we studied the effects of acute, physiologically relevant temperature changes on the density and kinetics of the L-type Ca(2+) channel current (I(Ca)) in rainbow trout atrial myocytes using the whole-cell patch-clamp technique. Myocytes from fish acclimated to 14 degrees C were first tested at 14 degrees C, then at 21 degrees C and finally at 7 degrees C. Using a square-pulse voltage-clamp in the first series of experiments, the peak density of I(Ca) increased (Q(10)=1.9) as temperature was increased from 14 to 21 degrees C and decreased (Q(10)=2.1) as temperature was decreased from 14 to 7 degrees C. In contrast to current density, the charge carried by I(Ca) was inversely related to temperature as a result of changes in the kinetic properties of the channel; both the fast (tau(f)) and slow (tau(s)) components of inactivation were slower at 7 degrees C than at 14 and 21 degrees C. Action potentials were recorded at the three test temperatures and then used as voltage-clamp stimulus waveforms to reassess I(Ca) in a second series of experiments. While the temperature-dependency of I(Ca) was similar to that found with the square-pulse voltage-clamp, the charge carried by I(Ca) was temperature-independent. These results show that the temperature-dependency of I(Ca) in rainbow trout is in the lower range of that reported in mammals and, although this could have profound effects on Ca(2+) delivery to the myofilaments, the temperature-induced modifications in the action potential may help to maintain a fairly constant Ca(2+) delivery during an acute temperature change in rainbow trout.

Differences in outward currents between neonatal and adult rabbit ventricular cells

1994 ◽  
Vol 266 (3) ◽  
pp. H1184-H1194 ◽  
Author(s):  
J. Sanchez-Chapula ◽  
A. Elizalde ◽  
R. Navarro-Polanco ◽  
H. Barajas
Keyword(s):  
Action Potential ◽  
Papillary Muscle ◽  
Action Potential Duration ◽  
Outward Current ◽  
Stimulation Frequency ◽  
Transient Outward Current ◽  
Adult Rabbit ◽  
Outward Currents ◽  
Recovery From Inactivation ◽  
In Cells

In adult rabbit ventricular preparations, action potential duration is significantly increased when stimulation frequency is increased from 0.1 to 1.0 Hz. In neonatal preparations, a similar change in stimulation frequency produced no significant increase in action potential duration. To identify the ionic basis for this difference, we studied different outward currents in single myocytes from papillary muscle and from epicardial tissue of adult and neonatal rabbits. The densities of the outward currents in neonatal cells were about one-half of the current density in adult cells. The density of the voltage-activated transient outward current (I(to1)) was smaller in cells from papillary muscle than in cells from epicardium in adult and newborn rabbits. We found major differences in the kinetic behavior of I(to1) between adult and neonatal cells: 1) the rate of apparent inactivation was faster in neonatal cells, and 2) the recovery from inactivation was significantly faster in neonatal cells, with a time constant of 113 vs. 1,356 ms. We propose that this marked difference in the recovery from inactivation of I(to1) is the basis for the difference in frequency dependence of action potential duration.

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