External K+ Concentration (external + k+_concentration)

Distribution by Scientific Domains


Selected Abstracts


Few cultured rat primary sensory neurons express a tolbutamide-sensitive K+ current

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2002
Violeta Ristoiu
Abstract The response of dorsal root ganglion (DRG) neurons to metabolic inhibition is known to involve calcium-activated K+ channels; in most neuronal types ATP-sensitive K+ channels (KATP) also contribute, but this is not yet established in the DRG. We have investigated the presence of a KATP current using whole-cell recordings from rat DRG neurons, classifying the neurons functionally by their "current signature" (Petruska et al, J Neurophysiol 84: 2365,2379, 2000). We clearly identified a KATP current in only 1 out of 62 neurons, probably a nociceptor. The current was activated by cyanide (2 mM NaCN) and was sensitive to 100 ,M tolbutamide; the relation between reversal potential and external K+ concentration indicated it was a K+ current. In a further two neurons, cyanide activated a K+ current that was only partially blocked by tolbutamide, which may also be an atypical KATP current. We conclude that KATP channels are expressed in normal DRG, but in very few neurons and only in nociceptors. [source]


NaCl-induced changes in cytosolic free Ca2+ in Arabidopsis thaliana are heterogeneous and modified by external ionic composition

PLANT CELL & ENVIRONMENT, Issue 8 2008
FRANCES E. TRACY
ABSTRACT Increases in cytosolic free Ca2+ ([Ca2+]cyt) are common to many stress-activated signalling pathways, including the response to saline environments. We have investigated the nature of NaCl-induced [Ca2+]cyt signals in whole Arabidopsis thaliana seedlings using aequorin. We found that NaCl-induced increases in [Ca2+]cyt are heterogeneous and mainly restricted to the root. Both the concentration of NaCl and the composition of the solution bathing the root have profound effects on the magnitude and dynamics of NaCl-induced increases in [Ca2+]cyt. Alteration of external K+ concentration caused changes in the temporal and spatial pattern of [Ca2+]cyt increase, providing evidence for Na+ -induced Ca2+ influx across the plasma membrane. The effects of various pharmacological agents on NaCl-induced increases in [Ca2+]cyt indicate that NaCl may induce influx of Ca2+ through both plasma membrane and intracellular Ca2+ -permeable channels. Analysis of spatiotemporal [Ca2+]cyt dynamics using photon-counting imaging revealed additional levels of complexity in the [Ca2+]cyt signal that may reflect the oscillatory nature of NaCl-induced changes in single cells. [source]


A voltage-dependent K+ current contributes to membrane potential of acutely isolated canine articular chondrocytes

THE JOURNAL OF PHYSIOLOGY, Issue 1 2004
Jim R. Wilson
The electrophysiological properties of acutely isolated canine articular chondrocytes have been characterized using patch-clamp methods. The ,steady-state' current,voltage relationship (I,V) of single chondrocytes over the range of potentials from ,100 to +40 mV was highly non-linear, showing strong outward rectification positive to the zero-current potential. Currents activated at membrane potentials negative to ,50 mV were time independent, and the I,V from ,100 to ,60 mV was linear, corresponding to an apparent input resistance of 9.3 ± 1.4 G, (n= 23). The outwardly rectifying current was sensitive to the K+ channel blocking ion tetraethylammonium (TEA), which had a 50% blocking concentration of 0.66 mm (at +50 mV). The ,TEA-sensitive' component of the outwardly rectifying current had time- and membrane potential-dependent properties, activated near ,45 mV and was half-activated at ,25 mV. The reversal potential of the ,TEA-sensitive' current with external K+ concentration of 5 mm and internal concentration of 145 mm, was ,84 mV, indicating that the current was primarily carried by K+ ions. The resting membrane potential of isolated chondrocytes (,38.1 ± 1.4 mV; n= 19) was depolarized by 14.8 ± 0.9 mV by 25 mm TEA, which completely blocked the K+ current of these cells. These data suggest that this voltage-sensitive K+ channel has an important role in regulating the membrane potential of canine articular chondrocytes. [source]


Effects of ouabain on contractions induced by manganese ions in Ca2+ -free, isotonic solutions with varying concentrations of K+ in guinea-pig taenia coli

FUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005
Tetsuyuki Nasu
Abstract The action of ouabain, a cell membrane Na+, K+ -ATPase blocker, on contractions induced by manganese ions (Mn2+) in Ca2+ -free, isotonic solutions with varying concentrations of K+ in the external medium were investigated in order to evaluate the underlying role of external Na+ in Mn2+ -induced contractions in isolated taenia coli of the guinea-pig. Mn2+ at 5 mm induced greater contractions as external isotonic K+ concentrations progressively increased from 10 to 100 mm. Ouabain (2 × 10,4 m) completely inhibited tension development stimulated by 5 mm Mn2+ in isotonic, 30 mm K+ (96 mm Na+) medium. Whereas, the tension inhibitory effects of ouabain became progressively weaker as isotonic, external K+ concentrations increased to 60 mm, which successively decreased external Na+ concentrations. Eventually, ouabain failed to affect contractions stimulated by Mn2+ in isotonic, 126 mm K+, Na+ -deficient medium. Ouabain caused progressively greater increase in cellular Na+ concentrations as the Na+ concentrations increased in the isotonic, K+ medium. While, pyruvate, which penetrates cell independently of external Na+, reversed the inhibition of tension by ouabain in isotonic, 30 mm K+, Na+ -sufficient (96 mm) medium containing 5 mm Mn2+. These results suggested that Mn2+ induced the contraction, which was maintained by glucose transport depending on external Na+, in the case of Na+ -sufficient medium in K+ -depolarized taenia coli. However, it induced the contraction independent of external Na+, in the case of Na+ -deficient, K+ medium. Ouabain might exhibit greater inhibition of the contraction induced by Mn2+ as the decrease in the Na+ gradient across the cell membranes continues. [source]