Time-dependent increase in Ca2+ influx in rabbit abdominal aorta: role of Na-Ca exchange

1993 ◽  
Vol 265 (5) ◽  
pp. C1325-C1331 ◽  
Author(s):  
M. A. Khoyi ◽  
R. A. Bjur ◽  
D. P. Westfall
Keyword(s):  
Abdominal Aorta ◽  
Sodium Pump ◽  
Time Dependent ◽  
Free Medium ◽  
Phorbol Dibutyrate ◽  
45Ca Fluxes ◽  
High K

Exposure of the rabbit abdominal aorta to the combination of high K+ and norepinephrine resulted in a time-dependent increase in the rate of 45Ca influx and 45Ca and 22Na content over that observed after stimulation with either K+ or norepinephrine alone. The increase in 45Ca influx, but not the increase in 22Na content, was extracellular Ca2+ (Cao2+) dependent. This time-dependent increase in 45Ca influx was prevented by incubating the tissue in Na(+)-free medium. Nifedipine inhibited both the initial depolarization-induced 45Ca influx and time-dependent increase in 45Ca influx and 22Na content. The effect of nifedipine on time-dependent fluxes was prevented by ouabain. Phorbol dibutyrate mimicked the effects of norepinephrine on 22Na retention and 45Ca fluxes. The effects of phorbol dibutyrate and norepinephrine were not additive. It is concluded that, in rabbit abdominal aorta, norepinephrine plus K+ causes 22Na retention (possibly through inhibition of the sodium pump) and a Cao(2+)- and intracellular Na+ (Nai+)-dependent increase in 45Ca influx. This latter effect is possibly the result of increased Nai(+)-Cao2+ exchange.

scholarly journals Peculiarities of time-dependent-dielectric breakdown characteristics of pure and doped Ta2O5 stacks

2013 ◽  
Vol 26 (3) ◽  
pp. 281-296
Author(s):  
E. Atanassova ◽  
A. Paskaleva
Keyword(s):  
Dielectric Breakdown ◽  
Interface Layer ◽  
Time Dependent ◽  
Relative Impact ◽  
Time Dependent Dielectric Breakdown ◽  
Breakdown Mechanism ◽  
Number Of Factors ◽  
High K ◽  
Induced Defects

The effect of both the process-induced defects and the dopant on the time-dependent-dielectric breakdown in Ta2O5 stacks is discussed. The breakdown degradation is analyzed in terms of specific properties of high-k stacks which make their dielectric breakdown mechanism completely different from that of classical SiO2. The relative impact of a number of factors constituting the reliability issues in Ta2O5-based capacitors (trapping in pre-existing traps, stress-induced new traps generation, the presence of interface layer at Si and the role of the dopant) is clarified.

scholarly journals The Role of Calcium in the Regulation of the Steady-State Levels of Sodium and Potassium in the HeLa Cell

1967 ◽  
Vol 50 (4) ◽  
pp. 781-792 ◽  
Author(s):  
Gene A. Morrill ◽  
Elliott Robbins
Keyword(s):  
Steady State ◽  
Free Medium ◽  
Na Transport ◽  
Cell Water ◽  
High K ◽  
Spinner Culture ◽  
Free Choline ◽  
Steady State Levels ◽  
Sodium And Potassium

Studies on HeLa cells in spinner culture at pH 7.0 and 37° have shown that [Na]i decreased and [K]i increased with increasing [Ca]o. In Na-free (choline) medium [K]i remained high whether or not Ca was present in the medium. [Na]i and [K]i approached a new steady state within 1 min after transfer to Ca-free medium and returned to the initial values within 15 min upon readdition of Ca. 40% of the cell Ca exchanged within 1 min followed by a slow exchange of the remaining Ca over several hours. [Ca]i increased with decreasing [Na]o but was independent of [K]o. Equimolar Mg did not substitute for Ca in maintaining low [Na]i and high [K]i. Under steady-state conditions about 50% of the cell Na exchanged in accordance with a single rate constant. The initial Na influx was 270, 100, and 2.5 µM/liter of cell water/sec for 0, 0.10, and 1.0 mM [Ca]o, respectively. When Na transport was inhibited with strophanthidin and [Na]i and [K]i allowed to reach a steady state, Na influx was more rapid for cells incubated in Ca-free medium than for cells incubated in medium containing 1.0 mM Ca. These results suggest that Ca competes with Na at the cell membrane and thus controls the passive diffusion of Na into the cell.

The role of Ca2+ in deflection-induced excitation of motile, mechanoresponsive balancer cilia in the ctenophore statocyst.

1997 ◽  
Vol 200 (11) ◽  
pp. 1593-1606 ◽  
Author(s):  
B Lowe
Keyword(s):  
Beat Frequency ◽  
Mnemiopsis Leidyi ◽  
Directional Sensitivity ◽  
Free Medium ◽  
Ciliary Beating ◽  
Graded Responses ◽  
Neural Input ◽  
High K ◽  
Pleurobrachia Pileus

Motile, mechanoresponsive cilia (balancers) in ctenophore statocysts, like vertebrate hair cells, are excited or inhibited depending upon the direction in which they are deflected. Balancers, however, may become either excited (beat rapidly) or inhibited (beat slowly) by deflection in the same direction, depending on the sign of ctenophore geotaxis (positive or negative). The beat frequency of many cilia is controlled by concentrations of Ca2+, membrane potential and neural input. How these factors affect deflection-induced ciliary beating in balancers was investigated. Deflection-induced excitation of balancers in whole Mnemiopsis leidyi larvae and dissected adult (Mnemiopsis leidyi, Pleurobrachia pileus) statocysts was reversibly inhibited by the Ca2+ channel inhibitors Co2+, Mg2+, Ni2+, and Mn2+. Deflection-induced excitation in balancers of isolated adult M. leidyi balancer groups was also inhibited by Co2+ or by Ca(2+)-free medium. Isolated balancer group cilia, like balancer cilia of intact ctenophores, exhibited responses to either sign of geotaxis and graded responses to deflection. Isolated balancers that were chemically depolarized in high-[K+], Ca(2+)-free medium were excited by local application of Ca2+ onto the ciliary bases, but not onto the cell bases or the ciliary tips. It is proposed that deflection-induced excitation of balancers is due to influx of Ca2+ through stretch- and voltage-activated channel activity. The sign of geotaxis of whole larvae and dissected adult statocysts was switched by electrical stimulation. Thus, neural input may participate in reversing the directional sensitivity of balancer cells.

scholarly journals The role of ATP in the differential ability of Sr2+ to trigger Ca2+ oscillations in mouse and human eggs

2021 ◽  
Author(s):  
Anna Storey ◽  
Khalil Elgmati ◽  
Yisu Wang ◽  
Paul Knaggs ◽  
Karl Swann
Keyword(s):  
Phospholipase C ◽  
Egg Activation ◽  
Apparent Difference ◽  
Free Medium ◽  
Inositol 1 ◽  
Atp Levels ◽  
Mature Mouse ◽  
Differential Ability ◽  
Mouse Eggs

Abstract At fertilization in mice and humans, the activation of the egg is caused by a series of repetitive Ca2+ oscillations which are initiated by phospholipase-C(zeta)ζ that generates inositol-1-4-5-trisphophate (InsP3). Ca2+ oscillations and egg activation can be triggered in mature mouse eggs by incubation in Sr2+ containing medium, but this does not appear to be effective in human eggs. Here we have investigated the reason for this apparent difference using mouse eggs, and human eggs that failed to fertilize after IVF or ICSI. Mouse eggs incubated in Ca2+-free, Sr2+-containing medium immediately underwent Ca2+ oscillations but human eggs consistently failed to undergo Ca2+ oscillations in the same Sr2+ medium. We tested the InsP3-receptor (IP3R) sensitivity directly by photo-release of caged InsP3 and found that mouse eggs were about 10 times more sensitive to InsP3 than human eggs. There were no major differences in the Ca2+ store content between mouse and human eggs. However, we found that the ATP concentration was consistently higher in mouse compared to human eggs. When ATP levels were lowered in mouse eggs by incubation in pyruvate-free medium, Sr2+ failed to cause Ca2+ oscillations. When pyruvate was added back to these eggs, the ATP levels increased and Ca2+ oscillations were induced. This suggests that ATP modulates the ability of Sr2+ to stimulate IP3R-induced Ca2+ release in eggs. We suggest that human eggs may be unresponsive to Sr2+ medium because they have a lower level of cytosolic ATP.

scholarly journals Endothelial cell-related autophagic pathways in Sugen/hypoxia-exposed pulmonary arterial hypertensive rats

2017 ◽  
Vol 313 (5) ◽  
pp. L899-L915 ◽  
Author(s):  
Fumiaki Kato ◽  
Seiichiro Sakao ◽  
Takao Takeuchi ◽  
Toshio Suzuki ◽  
Rintaro Nishimura ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Endothelial Cell ◽  
Vascular Remodeling ◽  
Time Dependent ◽  
Causative Role ◽  
Dependent Manner ◽  
Vascular Endothelial ◽  
Pulmonary Vascular Remodeling ◽  
Pulmonary Arterial

Pulmonary arterial hypertension (PAH) is characterized by progressive obstructive remodeling of pulmonary arteries. However, no reports have described the causative role of the autophagic pathway in pulmonary vascular endothelial cell (EC) alterations associated with PAH. This study investigated the time-dependent role of the autophagic pathway in pulmonary vascular ECs and pulmonary vascular EC kinesis in a severe PAH rat model (Sugen/hypoxia rat) and evaluated whether timely induction of the autophagic pathway by rapamycin improves PAH. Hemodynamic and histological examinations as well as flow cytometry of pulmonary vascular EC-related autophagic pathways and pulmonary vascular EC kinetics in lung cell suspensions were performed. The time-dependent and therapeutic effects of rapamycin on the autophagic pathway were also assessed. Sugen/hypoxia rats treated with the vascular endothelial growth factor receptor blocker SU5416 showed increased right ventricular systolic pressure (RVSP) and numbers of obstructive vessels due to increased pulmonary vascular remodeling. The expression of the autophagic marker LC3 in ECs also changed in a time-dependent manner, in parallel with proliferation and apoptotic markers as assessed by flow cytometry. These results suggest the presence of cross talk between pulmonary vascular remodeling and the autophagic pathway, especially in small vascular lesions. Moreover, treatment of Sugen/hypoxia rats with rapamycin after SU5416 injection activated the autophagic pathway and improved the balance between cell proliferation and apoptosis in pulmonary vascular ECs to reduce RVSP and pulmonary vascular remodeling. These results suggested that the autophagic pathway can suppress PAH progression and that rapamycin-dependent activation of the autophagic pathway could ameliorate PAH.

Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K+ in GH4C1 cells

1990 ◽  
Vol 123 (2) ◽  
pp. 218-224 ◽  
Author(s):  
Xiangbing Wang ◽  
Noriyuki Sato ◽  
Monte A. Greer ◽  
Susan E. Greer ◽  
Staci McAdams
Keyword(s):  
Smooth Muscle ◽  
Muscle Relaxant ◽  
Prolactin Secretion ◽  
Thyrotropin Releasing Hormone ◽  
Dependent Manner ◽  
Cell Toxicity ◽  
High K ◽  
Dose Dependent ◽  
Smooth Muscle Relaxant

Abstract. The mechanism by which 30% medium hyposmolarity induces PRL secretion by GH4C1 cells was compared with that induced by 100 nmol/l TRH or 30 mmol/l K+. Removing medium Ca2+, blocking Ca2+ channels with 50 μmol/l verapamil, or inhibiting calmodulin activation with 20 μmol/l trifluoperazine, 10 μmol/l chlorpromazine or 10 μmol/l pimozide almost completely blocked hyposmolarity-induced secretion. The smooth muscle relaxant, W-7, which is believed relatively specific in inhibiting the Ca2+-calmodulin interaction, depressed hyposmolarity-induced PRL secretion in a dose-dependent manner (r = −0.991, p<0.01 ). The above drugs also blocked or decreased high K+-induced secretion, but had much less effect on TRH-induced secretion. Secretion induced by TRH, hyposmolarity, or high K+ was optimal at pH 7.3-7.65 and was significantly depressed at pH 6.0 or 8.0, indicating that release of hormone induced by all 3 stimuli is due to an active cell process requiring a physiologic extracellular pH and is not produced by nonspecific cell toxicity. The data suggest hyposmolarity and high K+ may share some similarities in their mechanism of stimulating secretion, which is different from that of TRH.

scholarly journals Factors affecting the permeability of isolated fat-cells from the rat to [42K]potassium and [36Cl]chloride ions

1970 ◽  
Vol 117 (3) ◽  
pp. 615-621 ◽  
Author(s):  
M. C. Perry ◽  
C. N. Hales
Keyword(s):  
Initial Phase ◽  
Chloride Ions ◽  
Fat Cells ◽  
Adrenocorticotrophic Hormone ◽  
Isolated Fat Cells ◽  
Free Medium ◽  
Fat Cell ◽  
Factors Affecting ◽  
Exchange Diffusion ◽  
High K

1. The effluxes of 42K+ and 36Cl− from isolated fat-cells from the rat were studied under a variety of conditions known to affect the metabolism of the cells. 2. 42K+ efflux from isolated fat cells was increased in a Na+-free–high-K+ medium and decreased in a K+-free medium. The existence of K+ exchange diffusion across the fat-cell membrane is suggested. 3. 36Cl− efflux from isolated fat-cells was decreased when the Cl− component of the wash medium was replaced by acetate. The basal 36Cl− efflux is suggested to be partly by Cl− exchange diffusion and partly in company with a univalent cation. 4. A variety of lipolytic stimuli, adrenaline, adrenocorticotrophic hormone, N-6,O-2′-dibutyryladenosine cyclic 3′:5′-monophosphate and theophylline, increased 42K+ efflux from isolated fat-cells. The adrenaline stimulation was biphasic; an initial, rapid and transient increase in 42K+ loss from the fat-cells was followed by a slower, more prolonged, increase in 42K+ efflux. The initial phase was inhibited by phentolamine but not by propranolol. 5. Insulin increased 42K+ efflux only after preincubation with the cells.

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