Adjustment of osmotic pressure coupled with change of growth mode in Spirogyra

2008 ◽  
Vol 35 (7) ◽  
pp. 580 ◽  
Author(s):  
Katsuhisa Yoshida ◽  
Ai Ohtani ◽  
Tetsuro Mimura ◽  
Teruo Shimmen
Keyword(s):  
Osmotic Pressure ◽  
Tip Growth ◽  
Channel Blocker ◽  
Growth Mode ◽  
Terminal Cell ◽  
K Channel ◽  
Running Water ◽  
Intracellular Osmolarity ◽  
Cell Changes ◽  
External K

Spirogyra living in running water forms a rhizoid which anchors it to the substratum. Rhizoid differentiation can be induced in the laboratory by severing algal filaments. The terminal cell changes the growth mode from diffuse growth to tip growth, and finally differentiates to be a rhizoid. We found that the intracellular osmolarity of the rhizoid was significantly lower than that of other interjacent cells which did not form rhizoids. The decrease in the intracellular osmolarity began before the start of tip growth. TEA, a K+ channel blocker, inhibited the decrease in the intracellular osmolarity of the terminal cells; increase in the external K+ also inhibited this. It was suggested that K+ efflux through K+ channel is involved in the adjustment of osmotic pressure. When the adjustment of osmotic pressure was inhibited, tip growth did not start, inevitably, no rhizoid was formed. In Spirogyra sp. which was unable to form rhizoids, the terminal cell did not show the adjustment of osmotic pressure. Thus, this adjustment seems to be intimately coupled with the rhizoid differentiation. Possible roles of the adjustment of osmotic pressure in rhizoid differentiation are discussed.

Primary involvement of K+ conductance in membrane resonance of trigeminal root ganglion neurons

1988 ◽  
Vol 59 (1) ◽  
pp. 77-89 ◽  
Author(s):  
E. Puil ◽  
B. Gimbarzevsky ◽  
I. Spigelman
Keyword(s):  
Electrical Properties ◽  
Channel Blocker ◽  
Complex Impedance ◽  
Membrane Potentials ◽  
K Channel ◽  
Bathing Medium ◽  
Trigeminal Root ◽  
Membrane Resonance ◽  
Ganglion Neurons ◽  
Impedance Magnitude

1. The complex impedances and impedance magnitude functions were obtained from neurons in in vitro slices of trigeminal root ganglia using frequency-domain analyses of intracellularly recorded voltage responses to specified oscillatory input currents. A neuronal model derived from linearized Hodgkin-Huxley-like equations was used to fit the complex impedance data. This procedure yielded estimates for membrane electrical properties. 2. Membrane resonance was observed in the impedance magnitude functions of all investigated neurons at their initial resting membrane potentials and was similar to that reported previously for trigeminal root ganglion neurons in vivo. Tetrodotoxin (10(-6) M), a Na+-channel blocker, applied in the bathing medium for 20 min produced only minor changes, if any, in the resonance, although gross impairment of Na+-spike electrogenesis was apparent in most of the neurons. Brief applications (1-5 min) of a K+-channel blocker, tetraethylammonium (TEA; 10(-2) M), increased the impedance magnitude and abolished, in a reversible manner, the resonant behavior. In all cases, the resonant frequency was decreased by TEA administration prior to total blockade of resonance. 3. The TEA-induced blockade of resonance was associated with decreases in the estimates of the membrane conductances, without significant alterations of input capacitance. A particularly large decrease was observed in Gr, the time-invariant resting conductance that includes a lumped leak conductance component. The voltage- and time-dependent conductance, GL, and associated relaxation time constant, tau u, also declined progressively during administration of TEA. 4. Systematic variations in the membrane potentials of trigeminal root ganglion neurons were produced by intracellular injections of long-lasting step currents with superposition of the oscillatory current stimuli, in order to assess the effects of TEA on the relationship of the electrical properties to the membrane potential. Applications of TEA led to a depolarizing shift in the dependence of the membrane property estimates, suggesting voltage-dependence of the effects of TEA on presumed K+ channels in the membrane. 5. These data suggest a primary involvement of K+ conductance in the genesis of membrane resonance. This electrical behavior or its ionic mechanism is a major modulator of the subthreshold electrical responsiveness of trigeminal root ganglion neurons.

Arabidopsis AtCNGC10 rescues potassium channel mutants of E. coli, yeast and Arabidopsis and is regulated by calcium/calmodulin and cyclic GMP in E. coli

2005 ◽  
Vol 32 (7) ◽  
pp. 643 ◽  
Author(s):  
Xinli Li ◽  
Tamás Borsics ◽  
H. Michael Harrington ◽  
David A. Christopher
Keyword(s):  
Channel Blocker ◽  
K Channel ◽  
Structure Characteristic ◽  
Dependent Manner ◽  
Wild Type ◽  
Yeast Saccharomyces Cerevisiae ◽  
E Coli ◽  
Diverse Species ◽  
The Family ◽  
Low K

We have isolated and characterised AtCNGC10, one of the 20 members of the family of cyclic nucleotide (CN)-gated and calmodulin (CaM)-regulated channels (CNGCs) from Arabidopsis thaliana (L.) Heynh. AtCNGC10 bound CaM in a C-terminal subregion that contains a basic amphiphillic structure characteristic of CaM-binding proteins and that also overlaps with the predicted CN-binding domain. AtCNGC10 is insensitive to the broad-range K+ channel blocker, tetraethylammonium, and lacks a typical K+-signature motif. However, AtCNGC10 complemented K+ channel uptake mutants of Escherichia coli (LB650), yeast (Saccharomyces cerevisiae CY162) and Arabidopsis (akt1-1). Sense 35S-AtCNGC10 transformed into the Arabidopsis akt1-1 mutant, grew 1.7-fold better on K+-limited medium relative to the vector control. Coexpression of CaM and AtCNGC10 in E. coli showed that Ca2+ / CaM inhibited cell growth by 40%, while cGMP reversed the inhibition by Ca2+ / CaM, in a AtCNGC10-dependent manner. AtCNGC10 did not confer tolerance to Cs+ in E. coli, however, it confers tolerance to toxic levels of Na+ and Cs+ in the yeast K+ uptake mutant grown on low K+ medium. Antisense AtCNGC10 plants had 50% less potassium than wild type Columbia. Taken together, the studies from three evolutionarily diverse species demonstrated a role for the CaM-binding channel, AtCNGC10, in mediating the uptake of K+ in plants.

Enhanced role of K+ channels in relaxations of hypercholesterolemic rabbit carotid artery to NO

1995 ◽  
Vol 269 (3) ◽  
pp. H805-H811 ◽  
Author(s):  
S. Najibi ◽  
R. A. Cohen
Keyword(s):  
Carotid Artery ◽  
Sodium Nitroprusside ◽  
Channel Blocker ◽  
Isometric Tension ◽  
K Channel ◽  
K Channels ◽  
Rabbit Carotid Artery ◽  
Cyclic Monophosphate ◽  
Endothelium Dependent Relaxation

Endothelium-dependent relaxations to acetylcholine remain normal in the carotid artery of hypercholesterolemic rabbits, but unlike endothelium-dependent relaxations of normal rabbits, they are inhibited by charybdotoxin, a specific blocker of Ca(2+)-dependent K+ channels. Because nitric oxide (NO) is the mediator of endothelium-dependent relaxation and can activate Ca(2+)-dependent K+ channels directly or via guanosine 3',5'-cyclic monophosphate, the present study investigated the role of Ca(2+)-dependent K+ channels in relaxations caused by NO, sodium nitroprusside, and 8-bromoguanosine 3',5'-cyclic monophosphate (8-Brc-GMP) in hypercholesterolemic rabbit carotid artery. Isometric tension was measured in rabbit carotid artery denuded of endothelium from normal and hypercholesterolemic rabbits which were fed 0.5% cholesterol for 12 wk. Under control conditions, relaxations to all agents were similar in normal and hypercholesterolemic rabbit arteries. Charybdotoxin had no significant effect on relaxations of normal arteries to NO, sodium nitroprusside, or 8-BrcGMP, but the Ca(2+)-dependent K+ channel blocker significantly inhibited the relaxations caused by each of these agents in the arteries from hypercholesterolemic rabbits. By contrast, relaxations to the calcium channel blocker nifedipine were potentiated to a similar extent by charybdotoxin in both groups. In addition, arteries from hypercholesterolemic rabbits relaxed less than normal to sodium nitroprusside when contracted with depolarizing potassium solution. These results indicate that although nitrovasodilator relaxations are normal in the hypercholesterolemic rabbit carotid artery, they are mediated differently, and to a greater extent, by Ca(2+)-dependent K+ channels. These data also suggest that K+ channel-independent mechanism(s) are impaired in hypercholesterolemia.

scholarly journals Cibenzoline, an ATP-sensitive K+ channel blocker, binds to the K+ -binding site from the cytoplasmic side of gastric H+ ,K+ -ATPase

2001 ◽  
Vol 134 (8) ◽  
pp. 1655-1662 ◽  
Author(s):  
Yoshiaki Tabuchi ◽  
Hiroaki Yashiro ◽  
Satomi Hoshina ◽  
Shinji Asano ◽  
Noriaki Takeguchi
Keyword(s):  
Binding Site ◽  
Channel Blocker ◽  
K Channel ◽  
Cytoplasmic Side

Cl- fluxes related to fluid secretion by the rat parotid: involvement of Cl(-)-HCO3- exchange

1992 ◽  
Vol 262 (3) ◽  
pp. G393-G398 ◽  
Author(s):  
J. E. Melvin ◽  
R. J. Turner
Keyword(s):  
Channel Blocker ◽  
Kinetic Studies ◽  
Fluid Secretion ◽  
Disulfonic Acid ◽  
K Channel ◽  
Maximal Effect ◽  
Partial Recovery ◽  
Free Medium ◽  
Cl Channels ◽  
Rat Parotid

Muscarinic-induced 36Cl- and 86Rb+ (K+ substitute) fluxes were studied in rat parotid acini. Stimulation resulted in a rapid [half time (t1/2) less than 30 s] decrease in both Cl- and Rb+ content (approximately 50 and 30%, respectively) followed by a slower partial recovery (t1/2 approximately 3-4 min) to approximately 80% of resting levels for both ions. Cl- loss was inhibited by the venom of Leiurus quinquestriatus, which contains the maxi-K+ channel blocker charybdotoxin. Cl- recovery was blunted in the presence of bumetanide, an inhibitor of Na(+)-K(+)-Cl- cotransport, or on HCO3- removal and was completely blocked in the presence of bumetanide and 4,4' diisothiocyanostilbene-2,2' disulfonic acid (DIDS), an inhibitor of Cl(-)-HCO3- exchange. In HCO3(-)-containing medium a rapid (t1/2 less than 1 min), DIDS-inhibitable cytoplasmic alkalinization (approximately 0.4 pH unit) was observed in acini switched to a Cl(-)-free solution. This alkalinization was not seen in HCO3(-)-free medium but persisted in the absence of Na+, consistent with the presence of a potent Na(+)-independent Cl(-)-HCO3- exchanger. Kinetic studies indicated that the half-maximal effect of this exchanger for extracellular Cl- was approximately 18 mM. These results are consistent with the hypothesis that secretagogue-induced KCl loss by salivary acinar cells occurs via electrically coupled K+ and Cl- channels. In addition, they provide strong evidence that Cl- entry into, and thus fluid secretion by, these cells is mediated by both Cl(-)-HCO3- exchange and Na(+)-K(+)-Cl- cotransport.

Search for the pharmacophore of the K+ channel blocker, apamin

1991 ◽  
Vol 26 (9) ◽  
pp. 915-920 ◽  
Author(s):  
P Demonchaux ◽  
CR Ganellin ◽  
PM Dunn ◽  
DG Haylett ◽  
DH Jenkinson
Keyword(s):  
Channel Blocker ◽  
K Channel

The area and volume of single human erythrocytes during gradual osmotic swelling to hemolysis

1970 ◽  
Vol 48 (6) ◽  
pp. 369-376 ◽  
Author(s):  
Peter B. Canham ◽  
David R. Parkinson
Keyword(s):  
Osmotic Pressure ◽  
Single Cells ◽  
Ringer Solution ◽  
Potassium Ion ◽  
Distilled Water ◽  
Red Cell ◽  
Dialysis Membrane ◽  
Osmotic Swelling ◽  
Cell Changes ◽  
Area And Volume

A double-chambered slide was designed for the microscope which would enable continuous viewing of cells hanging on edge in a Ringer solution which was gradually being reduced in osmotic pressure. This was achieved by putting a dialysis membrane between the cell chamber and a chamber containing distilled water. Photographs were taken at 1-min intervals of single cells on edge (revealing the biconcave profile) until the cells hemolyzed, usually within 30 min. The area and volume of revolution of each cell were calculated from measurements on photographic enlargements. No significant change in area occurs during the swelling series although the red cell changes gradually from biconcave to spherical and remains spherical for approximately 7 min before hemolyzing. This stability is best explained by a leakage of potassium ion from the cell prior to hemolysis (which has been reported by Seeman to be approximately 20%).

Structure activity relationship studies on kaliotoxin, a peptidic K+ channel blocker

Peptides ◽  
1994 ◽  
pp. 529-531
Author(s):  
J. Van Rietschoten ◽  
R. Romi ◽  
M. Crest ◽  
F. Sampieri ◽  
H. Zerrouk ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Structure Activity Relationship ◽  
Activity Relationship ◽  
K Channel ◽  
Structure Activity

Solution-phase synthesis of the K+ channel blocker, charybdotoxin

Peptides 1990 ◽  
1991 ◽  
pp. 111-112
Author(s):  
Paul F. Lambert ◽  
Hisaya Kuroda ◽  
Naoyoshi Chino ◽  
Takushi X. Watanabe ◽  
Terutoshi Kimura ◽  
...  
Keyword(s):  
Channel Blocker ◽  
Solution Phase ◽  
K Channel ◽  
Phase Synthesis ◽  
Solution Phase Synthesis

Comparison of acetylcholine-dependent relaxation in large and small arteries of rat mesenteric vascular bed

1994 ◽  
Vol 266 (3) ◽  
pp. H952-H958 ◽  
Author(s):  
J. J. Hwa ◽  
L. Ghibaudi ◽  
P. Williams ◽  
M. Chatterjee
Keyword(s):  
Methylene Blue ◽  
Channel Blocker ◽  
Mesenteric Arteries ◽  
K Channel ◽  
Resistance Arteries ◽  
Vascular Bed ◽  
Mesenteric Vascular Bed ◽  
Relaxation Responses ◽  
Endothelium Dependent Relaxation

The relative contributions of nitric oxide (NO) to in vitro relaxation responses elicited by acetylcholine (ACh) were compared in vessels of different sizes from the rat mesenteric vascular bed. ACh elicited an endothelium-dependent relaxation in phenylephrine-contracted superior mesenteric arteries (SMA, unstretched luminal diam 650 microns), which was blocked by compounds that inhibited NO, such as hemoglobin (10 microM), methylene blue (10 microM), and NG-monomethyl-L-arginine (1 mM). In contrast, the endothelium-dependent relaxation induced by ACh in phenylephrine-contracted mesenteric resistance arteries (MRA, unstretched luminal diam 200 microns) was not blocked by hemoglobin, methylene blue, or NG-monomethyl-L-arginine. KCl (25 mM) partially inhibited the ACh-dependent relaxation in MRA. Furthermore, the ACh-dependent relaxation in MRA was selectively inhibited by the Ca(2+)-activated K+ channel blocker charybdotoxin (0.1 microM). In contrast, the ATP-sensitive K+ channel blocker glibenclamide (50 microM) did not block the ACh-dependent relaxation in MRA. We conclude that 1) NO is a major component of the ACh-dependent relaxation in SMA and 2) the ACh-dependent relaxation of MRA is resistant to NO inhibitors but sensitive to a Ca(2+)-activated K+ channel blocker. This suggests that an endothelium-derived hyperpolarization factor may be involved in the relaxation of MRA.

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