Calcium transients in identified leech glial cells in situ evoked by high potassium concentrations and 5-hydroxytryptamine

1992 ◽  
Vol 167 (1) ◽  
pp. 251-265 ◽  
Author(s):  
T. Munsch ◽  
J. W. Deitmer
Keyword(s):  
Cell Membrane ◽  
Glial Cells ◽  
Prolonged Exposure ◽  
Neuronal Cell ◽  
High Potassium ◽  
Fura 2 ◽  
Neuronal Cell Bodies ◽  
High K ◽  
K Concentration ◽  
External K

We have recorded the fluorescence of Fura-2-loaded, identified glial cells in the neuropile of the central nervous system of the leech Hirudo medicinalis using the ratio of emission at 350 nm excitation to that at 380 nm excitation as an indicator of intracellular Ca2+ concentration ([Ca2+]i). The neuropile glial cells were exposed by mechanically removing the overlying ganglionic capsule and the neuronal cell bodies and were then impaled using a microelectrode under visual control to inject Fura-2 ionophoretically. The resting Ca2+ level was measured using digitonin or Triton to permeabilize the cell membrane at different external concentrations of Ca2+; it was found to vary between 5 and 79 nmol l-1 and averaged 32 +/− 23 nmol l-1 (+/− S.D., N = 7). Raising the external K+ concentration from 4 to 20 mmol l-1 or adding 50 mumol l-1 5-hydroxytryptamine (5-HT) produced a rapid, reversible rise in [Ca2+]i. During prolonged exposure to high [K+] or 5-HT, [Ca2+]i remained high. Upon restoring normal external [K+] or removing 5-HT, [Ca2+]i returned to its initial resting value within 1–2 min. The responses of [Ca2+]i to high [K+] and 5-HT were greatly reduced in nominally Ca(2+)-free saline, suggesting that the [Ca2+]i transients required an influx of Ca2+ into the cells. In the presence of 5-HT, the rise in [Ca2+]i was accompanied by a decrease in the resistance and an increase in the responsiveness to K+ of the glial cell membrane, indicating the existence of a Ca(2+)-dependent K+ conductance elicited by 5-HT.

scholarly journals Effects of High Potassium and Low Temperature on the Growth and Magnesium Nutrition of Different Tomato Cultivars

HortScience ◽  
2018 ◽  
Vol 53 (5) ◽  
pp. 710-714 ◽  
Author(s):  
Huixia Li ◽  
Zhujun Chen ◽  
Ting Zhou ◽  
Yan Liu ◽  
Sajjad Raza ◽  
...  
Keyword(s):  
Low Temperature ◽  
Shoot Biomass ◽  
Total Biomass ◽  
High Potassium ◽  
Hydroponic Experiment ◽  
Root Shoot Ratio ◽  
High K ◽  
Significant Difference ◽  
Tomato Cultivars ◽  
K Concentration

The interaction between potassium (K) and magnesium (Mg) in plants has been intensively studied. However, the responses of different tomato (Solanum lycopersicum L.) cultivars to high K levels at low temperatures remained unclear. Herein, a complete randomized hydroponic experiment was conducted to evaluate the effects of temperature (25 °C day/18 °C night vs. 15 °C day/8 °C night) and K concentrations (156 mg·L−1 vs. 468 mg·L−1) on the growth and Mg nutrition of tomato cultivars Gailiangmaofen (MF) and Jinpeng No. 1 (JP). Compared with the control temperature (25 °C day/18 °C night), the low temperature decreased total biomass, shoot biomass, and Mg uptake in shoot by 17.3%, 24.1%, and 11.8%, respectively; however, the root/shoot ratio was increased. High K had no significant effect on plant growth or biomass compared with the control K concentration (156 mg·L−1); however, Mg concentrations and uptake in shoot were significantly lower under high-K treatment. Significant difference was observed for K uptake, but not for Mg uptake, between the two cultivars. There was no significant interaction between temperature and high K on Mg uptake of tomato, so a combined stress of low temperature and high K further inhibited Mg uptake and transport. Low temperature and high K increased the risk of Mg deficiency in tomato.

pH regulatory transport systems in a smooth muscle-like cell line

1990 ◽  
Vol 258 (3) ◽  
pp. C470-C479 ◽  
Author(s):  
R. W. Putnam
Keyword(s):  
Prolonged Exposure ◽  
Ph Regulation ◽  
Transport Systems ◽  
Disulfonic Acid ◽  
High K ◽  
Recovery From Acidification ◽  
Ethanesulfonic Acid ◽  
Membrane Transport Systems ◽  
External Ph ◽  
External K

The membrane transport systems responsible for pH regulation in BC3H-1 cells were studied using the pH-sensitive fluorescent dye 2',7'-bis(2-carboxyethyl)-5,6-carboxyfluorescein (BCECF). In nominally CO2-free Na N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid buffer (NHB) recovery from acidification after an NH4Cl pulse was reversibly inhibited by 1 mM amiloride or by Na-free solutions. On exposure to 5% CO2-HCO3 (external pH constant at 7.4), BC3H-1 cells alkalinized by approximately 0.3-0.4 pH unit. This CO2-induced alkalinization was unaffected by 1 mM amiloride, markedly reduced by 0.5 mM 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), and inhibited by Na-free solutions. On readdition of Na, cells rapidly alkalinized, even in the presence of 1 mM amiloride. Exposure to Cl-free CO2-HCO3 solutions caused a rapid alkalinization of nearly 1 pH unit that was abolished by SITS, largely independent of Na, unaffected by amiloride, and unchanged by membrane depolarization in high external K solutions. CO2-induced alkalinization was slowed by approximately 75% after prolonged exposure of cells to Cl-free NHB, but a distinct recovery from acidification remained in these Cl-depleted cells. This recovery was Na-dependent, SITS-inhibitable, and unaffected by depolarization in high-K solutions. In the presence of CO2, the acidification seen in response to NH4Cl-induced alkalinization was reduced 50% by 0.5 mM SITS. These data suggest that the regulation of pH in BC3H-1 cells is mediated by at least three transport systems: 1) Na-H exchange; 2) Cl-HCO3 exchange; and 3) electroneutral (Na + HCO3)-Cl exchange.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Brain spectrin(240/235) and brain spectrin(240/235E): two distinct spectrin subtypes with different locations within mammalian neural cells.

1986 ◽  
Vol 102 (6) ◽  
pp. 2088-2097 ◽  
Author(s):  
B M Riederer ◽  
I S Zagon ◽  
S R Goodman
Keyword(s):  
Blood Cell ◽  
Mouse Brain ◽  
Glial Cells ◽  
Red Blood Cell ◽  
Adult Mouse ◽  
Neuronal Cell ◽  
Neural Cells ◽  
Adult Mouse Brain ◽  
Neuronal Cell Bodies ◽  
Brain Spectrin

Adult mouse brain contains at least two distinct spectrin subtypes, both consisting of 240-kD and 235-kD subunits. Brain spectrin(240/235) is found in neuronal axons, but not dendrites, when immunohistochemistry is performed with antibody raised against brain spectrin isolated from enriched synaptic/axonal membranes. A second spectrin subtype, brain spectrin(240/235E), is exclusively recognized by red blood cell spectrin antibody. Brain spectrin(240/235E) is confined to neuronal cell bodies and dendrites, and some glial cells, but is not present in axons or presynaptic terminals.

Measurements of the Intracellular Potassium Activity of Retzius Cells in the Leech Central Nervous System

1981 ◽  
Vol 91 (1) ◽  
pp. 87-101
Author(s):  
JOACHIM W. DEITMER ◽  
WOLF R. SCHLUE
Keyword(s):  
Cell Membrane ◽  
External Solution ◽  
Equilibrium Potential ◽  
The Mean ◽  
K Concentration ◽  
Retzius Cells ◽  
Intracellular K Activity ◽  
K Permeability ◽  
K Activity ◽  
External K

The intracellular K activity of leech Retzius cells was measured using double-barrelled, liquid ion exchanger, microelectrodes. At the normal external K+ concentration of 4 mm (equivalent to 3 mm-K activity, assuming an activity coefficient of 0.75) the mean K activity was 101.3 ± 7.6 mm (S.D., n = 14) in the cell bodies, and 4.35 ± 0.4 mV (n = 27) in the extracellular spaces surrounding them, indicating a K+ equilibrium potential of - 80 mV. The mean membrane potential was - 43.6 + 4.9 mV (n = 14). In a K-free external solution, or in the presence of 5 × 10−4m-ouabain, the intracellular K activity decreased by up to 14 mm min−1. This indicates an efflux of K+ ions across the cell membrane of approximately 2 × 10−10 mol cm−2s, and an apparent K+ permeability coefficient of 8 × 10−8 cms−1. The cell membrane depolarized upon removal of K+ and upon addition of ouabain, and transiently hyperpolarized beyond its initial level on return to the normal external K+ concentration. The recovery from this hyperpolarization paralleled the increase of the intracellular K activity following the re-addition of K+. Our results suggest that, despite the high K+ permeability of the Retzius cell membrane, the intracellular K activity is maintained at a high level by an electrogenic pump.

Amiloride reduces potassium conductance in frog kidney via inhibition of Na+-H+ exchange

1986 ◽  
Vol 251 (1) ◽  
pp. F66-F73
Author(s):  
H. Oberleithner ◽  
G. Munich ◽  
A. Schwab ◽  
P. Dietl
Keyword(s):  
Cell Membrane ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Frog Kidney ◽  
High Potassium ◽  
Diluting Segment ◽  
Nephron Segment ◽  
Net Flux ◽  
Kidney Perfusion ◽  
K Concentration

The existence of a carrier-mediated Na+-H+ exchange has been described recently in many epithelial and nonepithelial tissues including the diluting segment of the amphibian kidney. In this preparation the Na+-H+ exchanger is dramatically stimulated by so-called K+ adaptation (chronic exposure of animals to high potassium) and completely inhibited by the diuretic drug amiloride. We performed electrophysiological experiments in diluting segments of the isolated perfused frog kidney to investigate whether amiloride affects the conductance properties of this epithelium. Amiloride dramatically increased the transepithelial resistance and the ratio of lumen over peritubular cell membrane resistance. Cell membrane potential changes, induced by luminal K+ concentration steps, were blunted by luminal application of amiloride, by luminal Na+-free perfusates, or by acidification of the kidney perfusion solution. K+ secretory net flux, measured by K+-sensitive microelectrodes, decreased by half in presence of the diuretic. The experiments reveal that amiloride reduces the K+ conductance of the luminal cell membrane of frog diluting segment via inhibition of the luminal Na+-H+ exchanger. This decreases transepithelial K+ net secretion in this nephron segment.

The α-action of catecholamines on the guinea-pig taenia coli in K-free and Na-free solution and in the presence of ouabain

1977 ◽  
Vol 197 (1128) ◽  
pp. 255-269 ◽  
Keyword(s):  
Guinea Pig ◽  
Prolonged Exposure ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Taenia Coli ◽  
Free Solution ◽  
Na Pump ◽  
K Concentration ◽  
External K

The responses of guinea-pig taenia coli to the α-action of adrenaline and noradrenaline, recorded with the double sucrose-gap method, were ( a ) studied in conditions which inhibit Na-pump activity (exposure to 0 K, 0 Na, ouabain, low temperature) and ( b ) compared with the effect of Na-pump activation (readmission of K after prolonged exposure to 0 K). When the external K concentration was modified, the alteration of the change in membrane potential produced by the catecholamines was as would be expected from the shift of the K-equilibrium potential. The decrease in the membrane resistance was greater in a high external K con­centration and smaller in K-free solution. Readmission of K after prolonged exposure to K-free solution produced a large hyperpolarization, but, in the presence of ouabain (5 × 10 -5 M) or in the absence of Na, K readmission produced depolarization. In contrast, the effects of adrenaline and noradrenaline were not essentially modified by ouabain, nor by removal of Na. Reduction of the external K concentration enhanced the hyperpolarization by catecholamines even in the presence of ouabain or in the absence of external Na. During prolonged exposure to adrenaline or noradrenaline (7min) the increase in membrane conductance and the hyperpolarization of the membrane were largely maintained, though there was some spontaneous recovery in the presence of the catecholamines. These long-lasting respon­ses were essentially the same when the temperature was lowered from 37 to 20°C, and also in the presence of ouabain. All the results obtained were unaffected by the presence or absence of propranolol. It was concluded that the hyperpolarization produced by the α-action of catecholamines did not involve an activation of the Na-pump but was mainly caused by an increase in the K conductance of the membrane.

scholarly journals Potassium-sparing effects of furosemide in mice on high-potassium diets

2019 ◽  
Vol 316 (5) ◽  
pp. F970-F973
Author(s):  
Bangchen Wang ◽  
Steven C. Sansom
Keyword(s):  
Bk Channel ◽  
Na Channel ◽  
Thick Ascending Limb ◽  
Distal Nephron ◽  
High Potassium ◽  
Henle's Loop ◽  
High K ◽  
K Secretion ◽  
K Concentration ◽  
Sites Of Action

In individuals on a regular “Western” diet, furosemide induces a kaliuresis and reduction in plasma K concentration by inhibiting Na reabsorption in the thick ascending limb of Henle’s loop, enhancing delivery of Na to the aldosterone-sensitive distal nephron. In the aldosterone-sensitive distal nephron, the increased Na delivery stimulates K wasting due to an exaggerated exchange of epithelial Na channel-mediated Na reabsorption of secreted K. The effects of furosemide are different in mice fed a high-K, alkaline (HK) diet: the large-conductance Ca-activated K (BK) channel, in conjunction with the BK β4-subunit (BK-α/β4), mediates K secretion from intercalated cells (IC) of the connecting tubule and collecting ducts. The urinary alkaline load is necessary for BK-α/β4-mediated K secretion in HK diet-fed mice. However, furosemide acidifies the urine by increasing vacuolar ATPase expression and acid secretion from IC, thereby inhibiting BK-α/β4-mediated K secretion and sparing K. In mice fed a low-Na, high-K (LNaHK) diet, furosemide causes a greater increase in plasma K concentration and reduction in K excretion than in HK diet-fed mice. Micropuncture of the early distal tubule of mice fed a LNaHK diet, but not a regular or a HK diet, reveals K secretion in the thick ascending limb of Henle’s loop. The sites of action of K secretion in individuals consuming a high-K diet should be taken into account when diuretic agents known to waste K with low or moderate K intakes are prescribed.

Potassium loss from hypoxic myocardium: influence of external K concentration

1987 ◽  
Vol 65 (5) ◽  
pp. 861-866 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti ◽  
Denis Chartier
Keyword(s):  
Electrical Activity ◽  
Sodium Content ◽  
Total Water ◽  
Tissue Samples ◽  
Normal Medium ◽  
High K ◽  
Voltage Dependent ◽  
External Potassium ◽  
K Concentration ◽  
External K

The influence of external potassium Ko and tetraethylammonium on the cellular K content of hypoxic myocardium was investigated. Perfused rabbit hearts were submitted to 60 min hypoxia in medium containing 5 mM K throughout or either low (1.5 mM) or high (10 mM) K during the last 20 min of hypoxia. Paced electrical activity (2.5 Hz) was kept throughout the experiments. Tissue samples excised from the left ventricle were analyzed for total water, inulin space, and Na and K content. Lowering Ko to 1.5 mM increased both K loss and Na accumulation. Addition of 3.5 mM RbCl under these conditions reversed Na accumulation to levels found for hypoxia in normal medium but did not modify the cellular K loss. Tetraethylammonium (10 mM) did not alter Na accumulation but partly prevented the decrease in K content produced by hypoxia. A similar effect was observed by increasing Ko to 10 mM. At this high Ko prolongation of hypoxia did not enhance K loss. Abolition of electrical activity by TTX in a high K solution prevented K loss and reduced the sodium content. These results are consistent with the view that voltage-dependent channels are implicated in the K loss induced by hypoxia or ischemia. Furthermore, they indicate that the K loss may be modulated by external K because of the influence of the electrochemical gradient on passive K efflux and thus provide an explanation for the existence of a plateau in the early extracellular K accumulation observed during cardiac ischemia.

K+-stimulated sugar uptake in skeletal muscle: role of cytoplasmic Ca2+

1983 ◽  
Vol 245 (1) ◽  
pp. C125-C132 ◽  
Author(s):  
P. Valant ◽  
D. Erlij
Keyword(s):  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Cytochalasin B ◽  
Sugar Transport ◽  
Sugar Uptake ◽  
Frog Skeletal Muscle ◽  
High K ◽  
K Concentration ◽  
External K

We have compared the effects of insulin with those of elevated external K+ concentration ([K+]o) on sugar uptake and protein synthesis by frog skeletal muscle. When [K+]o was between 0.5 and 15 mM there were no effects on uptake; however, when 20 mM was used a significant increase was observed. Further increases in [K+]o caused larger stimulations of uptake. The stimulation persisted for 2.5 h after washing the high [K+]o. The stimulations caused by both insulin and high K+ were markedly inhibited by cytochalasin B. Dantrolene nearly abolished the response to high K+, whereas it had only minor effects on the resting sugar uptake and on the stimulations caused by either insulin or epinephrine. These results suggest that while both insulin and high K+ activate the cytochalasin-sensitive transport system of sugar transport, each agent must act through a different pathway, because only the effects of high K+ were dantrolene sensitive. The effect of dantrolene suggests that the enhancement of sugar transport caused by high K+ is due to an increase of cytoplasmic Ca2+. In contrast to insulin, high K+ did not modify the rate of protein synthesis.

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