Effect of osmolality on cytosolic free calcium and aldosterone secretion

1992 ◽  
Vol 262 (1) ◽  
pp. E68-E75 ◽  
Author(s):  
W. Wang ◽  
N. Hayama ◽  
T. V. Robinson ◽  
R. E. Kramer ◽  
E. G. Schneider
Keyword(s):  
Calcium Influx ◽  
Potassium Concentration ◽  
Sodium Concentration ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Free Calcium ◽  
Aldosterone Secretion ◽  
Voltage Dependent ◽  
Glomerulosa Cells ◽  
Dose Dependent

Alterations in extracellular osmolality have powerful inverse effects on basal and potassium- and angiotensin-stimulated aldosterone secretion. With the use of bovine glomerulosa cells grown in primary culture, the effects of alterations in osmolality on cytosolic calcium concentration ([Ca2+]c), efflux and uptake of 45Ca2+, and aldosterone secretion were determined. Alterations in osmolality, independent of sodium concentration, have inverse effects on aldosterone secretion, which are correlated with simultaneous changes in [Ca2+]c measured using fura-2. Reductions in osmolality cause dose-dependent biphasic increases in [Ca2+]c different from the monophasic increases in [Ca2+]c produced by increases in potassium concentration. Like potassium- and angiotensin-stimulated increases in [Ca2+]c, hypotonically induced increases in [Ca2+]c are associated with an increase in 45Ca2+ efflux. Reductions in osmolality also increased the uptake of 45Ca2+, an effect apparent at 2 min and persistent for at least 30 min. In the absence of extracellular calcium, reductions in osmolality, as increases in potassium concentration but not angiotensin, fail to increase [Ca2+]c, efflux of 45Ca2+, or aldosterone secretion. In conclusion, osmolality-induced alterations in aldosterone secretion are associated with parallel changes in [Ca2+]c, effects caused by alteration in the influx of extracellular calcium. On the basis of these and previous studies, we hypothesize that osmolality affects calcium influx by activating voltage-dependent or stretch-activated calcium channels.

Potassium-induced aldosterone secretion involves a Cl(-)-dependent mechanism

1997 ◽  
Vol 272 (1) ◽  
pp. R183-R187 ◽  
Author(s):  
W. Wang ◽  
E. G. Schneider
Keyword(s):  
Cell Volume ◽  
Calcium Concentration ◽  
Potassium Concentration ◽  
Chloride Ion ◽  
Cytosolic Calcium ◽  
Extracellular Potassium ◽  
Aldosterone Secretion ◽  
Extracellular Potassium Concentration ◽  
Glomerulosa Cells ◽  
Dependent Mechanism

Stimulation of aldosterone secretion by increases in extracellular potassium concentration is associated with increases in the volume of the adrenal glomerulosa cell. Because increases in cell volume have been associated with increases in aldosterone secretion, the effect of preventing the potassium-induced increase in cell volume by removal of chloride from the medium on the response of dispersed bovine glomerulosa cells grown in primary culture was determined. Totally replacing the chloride ion with the methylsulfate ion prevented the increase in cell volume and significantly suppressed the increase in aldosterone secretion normally associated with increasing [K] to 10 mM. In the absence of Cl-, the increase in cytosolic calcium concentration ([Ca2+]c) normally induced by increasing the [K] to 10 mM was also significantly suppressed. The replacement of 10 mM methylsulfate by Cl- restored the potassium-induced increase in both cell volume and aldosterone secretion to values not different from those found in the presence of 108 mM Cl-. The potassium-induced increase in cell volume was dependent also on the presence of extracellular calcium. Thus a component of the glomerulosa cell response to an increase in [K] may be caused by a chloride-dependent increase in cell volume that is triggered by the initial depolarization-induced increase in [Ca2+]c. The increase in cell volume enhances the increase in [Ca2+]c and amplifies the increase in aldosterone secretion.

scholarly journals Effects of extracellular calcium and potassium on the sodium pump of rat adrenal glomerulosa cells

2001 ◽  
Vol 280 (1) ◽  
pp. C119-C125 ◽  
Author(s):  
Douglas R. Yingst ◽  
Joanne Davis ◽  
Rick Schiebinger
Keyword(s):  
Sodium Pump ◽  
Calcium Influx ◽  
Calcium Ionophore ◽  
Extracellular Calcium ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Extracellular Potassium ◽  
A 23187 ◽  
Pump Activity ◽  
Glomerulosa Cells

Because the activity of the sodium pump (Na-K-ATPase) influences the secretion of aldosterone, we determined how extracellular potassium (Ko) and calcium affect sodium pump activity in rat adrenal glomerulosa cells. Sodium pump activity was measured as ouabain-sensitive 86Rb uptake in freshly dispersed cells containing 20 mM sodium as measured with sodium-binding benzofluran isophthalate. Increasing Ko from 4 to 10 mM in the presence of 1.8 mM extracellular calcium (Cao) stimulated sodium pump activity up to 165% and increased intracellular free calcium as measured with fura 2. Increasing Ko from 4 to 10 mM in the absence of Cao stimulated the sodium pump ∼30% and did not increase intracellular free calcium concentration ([Ca2+]i). In some experiments, addition of 1.8 mM Cao in the presence of 4 mM Ko increased [Ca2+]i above the levels observed in the absence of Cao and stimulated the sodium pump up to 100%. Ca-dependent stimulation of the sodium pump by Ko and Cao was inhibited by isradipine (10 μM), a blocker of L- and T-type calcium channels, by compound 48/80 (40 μg/ml) and calmidizolium (10 μM), which inhibits calmodulin (CaM), and by KN-62 (10 μM), which blocks some forms of Ca/CaM kinase II (CaMKII). Staurosporine (1 μM), which effectively blocks most forms of protein kinase C, had no effect. In the presence of A-23187, a calcium ionophore, the addition of 0.1 mM Cao increased [Ca2+]i to the level observed in the presence of 10 mM Ko and 1.8 mM Cao and stimulated the sodium pump 100%. Ca-dependent stimulation by A-23187 and 0.1 mM Cao was not reduced by isradipine but was blocked by KN-62. Thus, under the conditions that Ko stimulates aldosterone secretion, it stimulates the sodium pump by two mechanisms: direct binding to the pump and by increasing calcium influx, which is dependent on Cao. The resulting increase in [Ca2+]i may stimulate the sodium pump by activating CaM and/or CaMKII.

Sevoflurane but not propofol provided dual effects of cell survival in human neuroblastoma SH-SY5Y cells

2021 ◽  
Vol 18 ◽  
Author(s):  
Xue Gao ◽  
Xiu Wang ◽  
Lei Zhang ◽  
Ge Liang ◽  
Rachel Mund ◽  
...  
Keyword(s):  
Cell Survival ◽  
Prolonged Exposure ◽  
Calcium Influx ◽  
Cell Damage ◽  
Cytosolic Calcium ◽  
Extracellular Calcium ◽  
Mitochondrial Calcium ◽  
General Anesthetics ◽  
Wild Type ◽  
Human Neuroblastoma

Background: We have hypothesized that the most commonly used intravenous (propofol) and inhalational (sevoflurane) general anesthetics affect cell survival concentration and duration dependently with different potency associated with their differential potency to affect intracellular calcium homeostasis. Methods: Human neuroblastoma SH-SY5Y cells stably transfected with either wild type or M146L mutant human presenilin 1 were cultured and exposed to equipotent of propofol or sevoflurane. Cell viability, cytosolic and mitochondrial calcium were measured. Results: Sevoflurane but not propofol, at clinically relevant concentrations and durations, promoted cell survival. Prolonged exposure (24 hours) of 1% sevoflurane resulted in significant cell damage in both types of cells. Both sevoflurane and propofol had significantly higher cell response rates to the elevation of cytosolic calcium or mitochondrial calcium in the presence of extracellular calcium. With the contribution of calcium influx, sevoflurane but not equipotent 1 MAC propofol, caused a significantly greater increase in peak and overall calcium in Alzheimer’s mutation cell than in wild type cells, but significantly more increase in overall mitochondrial calcium concentrations in wild type than mutation cells. In the absence of extracellular calcium influx, sevoflurane, but not propofol, caused more significant elevations of overall mitochondrial calcium concentration in mutation cells than control cells. Conclusion: Calcium influx contributed to the general anesthetics mediated elevation of cytosolic or mitochondrial calcium, which is especially true for propofol. Sevoflurane has a greater potency to either promote or inhibit cell survival than propofol, which may be associated with its ability to affect cytosolic or mitochondrial calcium.

scholarly journals Direct modulation of basal and angiotensin II-stimulated aldosterone secretion by hydrogen ions

2000 ◽  
Vol 166 (1) ◽  
pp. 183-194 ◽  
Author(s):  
RE Kramer ◽  
TV Robinson ◽  
EG Schneider ◽  
TG Smith
Keyword(s):  
Angiotensin Ii ◽  
Free Calcium ◽  
Acid Base Balance ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Low Concentrations ◽  
Effects Of Ph ◽  
Glomerulosa Cells

Disturbances in acid-base balance in vivo are associated with changes in plasma aldosterone concentration, and in vitro changes in extracellular pH (pH(o)) influence the secretion of aldosterone by adrenocortical tissue or glomerulosa cells. There is considerable disparity, however, as to the direction of the effect. Furthermore, the mechanisms by which pH(o) independently affects aldosterone secretion or interacts with other secretagogues are not defined. Thus, bovine glomerulosa cells maintained in primary monolayer culture were used to examine the direct effects of pH(o) on cytosolic free calcium concentration ([Ca(2+)](i))( )and aldosterone secretion under basal and angiotensin II (AngII)-stimulated conditions. pH(o) was varied from 7.0 to 7.8 (corresponding inversely to changes in extracellular H(+) concentration from 16 nM to 100 nM). Whereas an elevation of pH(o) from 7.4 to 7.8 had no consistent effect, reductions of pH(o) from 7.4 to 7.2 or 7.0 caused proportionate increases in aldosterone secretion that were accompanied by increases in transmembrane Ca(2+) fluxes and [Ca(2+)](i). These effects were abolished by removal of extracellular Ca(2+). A decrease in pH(o) from 7.4 to 7.0 also enhanced AngII-stimulated aldosterone secretion. This effect was more pronounced at low concentrations of AngII and was manifested as an increase in the magnitude of the secretory response with no effect on potency. In contrast to its effect on AngII-stimulated aldosterone secretion, a reduction of pH(o) from 7.4 to 7.0 inhibited the Ca(2+) signal elicited by low concentrations (</=1x10(-10) M) of AngII, but did not affect the increase in [Ca(2+)](i) caused by a maximal concentration (1x10(-8) M) of AngII. These data suggest that pH(o) (i.e. H(+)) has multiple effects on aldosterone secretion. It independently increases aldosterone secretion through a mechanism involving Ca(2+) influx and an increase in [Ca(2+)](i). Also, it modulates the action of AngII by both decreasing the magnitude of the AngII-stimulated Ca(2+) signal and increasing the sensitivity of a more distal site to intracellular Ca(2+). The latter action appears to be a more important determinant in the effects of pH(o) on AngII-stimulated aldosterone secretion.

Effectiveness of the aldosterone-sodium and -potassium feedback control system

1976 ◽  
Vol 231 (3) ◽  
pp. 945-953 ◽  
Author(s):  
DB Young ◽  
RE McCaa ◽  
UJ Pan ◽  
AC Guyton
Keyword(s):  
Feedback Control ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Plasma Potassium ◽  
Sodium Concentration ◽  
Feedback Mechanism ◽  
Fluid Volume ◽  
The Body ◽  
Plasma Sodium ◽  
Aldosterone Secretion

This study was conducted to determine the quantitative importance of the aldosterone feedback mechanism in controlling each one of three major factors that have often been associated with aldosterone, namely, extracellular fluid sodium concentration, extracellular fluid potassium concentration, and extracellular fluid volume. To do this, the ability of the body to control these three factors in the face of marked changes in daily sodium or potassium intake was studied under two conditions: 1) in the normal dog, and 2) in the dog in which the aldosterone feedback mechanism was prevented from functioning by removing the adrenal glands and then providing a continuous fixed level of supportive aldosterone and glucocorticoids during the low and high electrolyte intake periods. Under these conditions, removal of feedback control of aldosterone secretion decreased the effectiveness of plasma potassium control by nearly fivefold (39% vs. 8% change in plasma potassium concentration), fluid volume by sixfold (12% vs. 2% change in sodium space) and had no effect on control of plasma sodium concentration (2% change with and without feedback control of aldosterone secretion.)

Angiotensin II causes sustained elevations in cytosolic calcium in glomerulosa cells

1988 ◽  
Vol 255 (3) ◽  
pp. E338-E346 ◽  
Author(s):  
R. E. Kramer
Keyword(s):  
Angiotensin Ii ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Cytosolic Calcium Concentration ◽  
Free Calcium Concentration ◽  
Cytosolic Free Calcium Concentration ◽  
Glomerulosa Cells

Studies were conducted to examine the effects of angiotensin II on cytosolic free calcium concentration in bovine adrenal glomerulosa cells maintained in primary culture. The calcium indicator, fura-2, and discontinuous dual-wavelength fluorescence spectroscopy were used to measure cytosolic free calcium in superfused adherent cell monolayers. Basal cytosolic free calcium concentration was 63.7 +/- 3.3 nM. The threshold concentration for angiotensin II-stimulated increases in cytosolic calcium was 10(-14)-10(-13) M, and maximal elevation of cytosolic calcium was produced by 10(-9) M angiotensin II. Angiotensin II (10(-13) M) produced a gradual increase in cytosolic calcium concentration that plateaued after 3-5 min of superfusion at a level approximately 1.2 times that of control cells. The calcium signal invoked by a maximal concentration (10(-9) M) of angiotensin II, in contrast, was characterized by an immediate, intense (approximately 8-fold) increase in cytosolic calcium concentration that decayed within 5 min to a lower, but sustained, level 2.5-3 times that of control cells. The calcium signals invoked by intermediate concentrations (10(-12)-10(-10) M) of angiotensin II exhibited dose-dependent increases in magnitude and a gradual transition in nature between those invoked by threshold and maximal concentrations of the peptide. The effect of angiotensin II to increase cytosolic calcium concentration was accompanied by an increase in aldosterone output. The increase in steroidogenesis was most closely correlated with the magnitude of the initial calcium signal. At high concentrations (10(-10) and 10(-9) M) of angiotensin II, there was a clear dissociation between aldosterone output and the magnitude of the sustained calcium signal.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Mechanism of inhibitory action of TMB-8 [8-(NN-diethylamino)octyl-3,4,5-trimethoxybenzoate] on aldosterone secretion in adrenal glomerulosa cells

1985 ◽  
Vol 232 (1) ◽  
pp. 87-92 ◽  
Author(s):  
I Kojima ◽  
K Kojima ◽  
H Rasmussen
Keyword(s):  
Protein Kinase C ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Calcium Release ◽  
Calcium Influx ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Aldosterone Secretion ◽  
Kinase C ◽  
Glomerulosa Cells

The mechanism of 8-(NN-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) action was evaluated in isolated adrenal glomerulosa cells. TMB-8 inhibits both angiotensin II- and K+-stimulated aldosterone secretion in a dose-dependent manner. The ID50 for angiotensin II- and K+-stimulated aldosterone secretion is 46 and 28 microM, respectively. In spite of the fact that 100 microM-TMB-8 inhibits angiotensin II-stimulated aldosterone secretion almost completely, TMB-8 (100 microM) does not inhibit angiotensin II-induced 45Ca2+ efflux from prelabelled cells nor does it affect inositol 1,4,5-trisphosphate-induced calcium release from non-mitochondrial pool(s) in saponin-permeabilized cells. TMB-8 has no inhibitory effect on A23187-induced aldosterone secretion, but 12-O-tetradecanoylphorbol 13-acetate-induced aldosterone secretion is completely abolished. TMB-8 effectively inhibits both angiotensin II- and K+-induced increases in calcium influx but has no effect on A23187-induced calcium influx. TMB-8 inhibits the activity of protein kinase C dose-dependently. These results indicate that TMB-8 inhibits aldosterone secretion without inhibiting mobilization of calcium from an intracellular pool. The inhibitory effect of TMB-8 is due largely to an inhibition of plasma membrane calcium influx, but this drug also inhibits the activity of protein kinase C directly.

Mechanisms of cytosolic calcium elevation in plants: the role of ion channels, calcium extrusion systems and NADPH oxidase-mediated 'ROS-Ca2+ Hub'

2018 ◽  
Vol 45 (2) ◽  
pp. 9 ◽  
Author(s):  
Vadim Demidchik ◽  
Sergey Shabala
Keyword(s):  
Calcium Influx ◽  
Gene Families ◽  
Cytosolic Calcium ◽  
Recent Experimental Data ◽  
Free Calcium ◽  
Cyclic Nucleotide Gated Channels ◽  
Physiological Reactions ◽  
Calcium Extrusion ◽  
Calcium Elevation

Elevation in the cytosolic free calcium is crucial for plant growth, development and adaptation. Calcium influx into plant cells is mediated by Ca2+ depolarisation-activated, hyperpolarisation-activated and voltage-independent Ca2+-permeable channels (DACCs, HACCs and VICCs respectively). These channels are encoded by the following gene families: (1) cyclic nucleotide-gated channels (CNGCs), (2) ionotropic glutamate receptors (GLRs), (3) annexins, (4) ‘mechanosensitive channels of small (MscS) conductance’-like channels (MSLs), (5) ‘mid1-complementing activity’ channels (MCAs), Piezo channels, and hyperosmolality-induced [Ca2+]cyt. channel 1 (OSCA1). Also, a ‘tandem-pore channel1’ (TPC1) catalyses Ca2+ efflux from the vacuole in response to the plasma membrane-mediated Ca2+ elevation. Recent experimental data demonstrated that Arabidopsis thaliana (L.) Heynh. CNGCs 2, 5–10, 14, 16 and 18, GLRs 1.2, 3.3, 3.4, 3.6 and 3.7, TPC1, ANNEXIN1, MSL9 and MSL10,MCA1 and MCA2, OSCA1, and some their homologues counterparts in other species, are responsible for Ca2+ currents and/or cytosolic Ca2+ elevation. Extrusion of Ca2+ from the cytosol is mediated by Ca2+-ATPases and Ca2+/H+ exchangers which were recently examined at the level of high resolution crystal structure. Calcium-activated NADPH oxidases and reactive oxygen species (ROS)-activated Ca2+ conductances form a self-amplifying ‘ROS-Ca2+hub’, enhancing and transducing Ca2+ and redox signals. The ROS-Ca2+ hub contributes to physiological reactions controlled by ROS and Ca2+, demonstrating synergism and unity of Ca2+ and ROS signalling mechanisms.

Unique calcium dependencies of the activating mechanism of the early and late aldosterone biosynthetic pathways in the rat

1986 ◽  
Vol 110 (2) ◽  
pp. 315-325 ◽  
Author(s):  
R. J. Schiebinger ◽  
L. M. Braley ◽  
A. Menachery ◽  
G. H. Williams
Keyword(s):  
Angiotensin Ii ◽  
Calcium Channel ◽  
Biosynthetic Pathway ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Aldosterone Secretion ◽  
Calcium Dependency ◽  
Pathway Activation ◽  
Dihydropyridine Calcium Channel Antagonist ◽  
Channel Dependent

ABSTRACT This study compared the extracellular calcium dependency and the enzymatic locus of that dependency for N6,O2′-dibutyryl cyclic AMP (dbcAMP)-, angiotensin II- and potassium-stimulated aldosterone secretion in dispersed rat glomerulosa cells. The need for extracellular calcium, calcium influx, and specifically for calcium influx through the calcium channel was examined. dbcAMP, angiotensin II and potassium, in the presence of calcium (3·5 mmol/l), significantly (P < 0·01) increased aldosterone output by at least 1·5-fold. Yet in the absence of extracellular calcium or in the presence of lanthanum (an inhibitor of calcium influx by most mechanisms) all three stimuli failed to increase aldosterone secretion. Nifedipine, a dihydropyridine calcium channel antagonist, significantly (P < 0·01) reduced angiotensin II- and potassium-stimulated aldosterone secretion, but had no effect on dbcAMP-stimulated aldosterone secretion (100 ± 14 vs 105 ± 19 pmol/106 cells). Likewise nitrendipine failed to inhibit ACTH-stimulated aldosterone secretion. Angiotension II and potassium activation of both the early aldosterone biosynthetic pathway (as reflected by pregnenolone production in the presence of cyanoketone) and also its late pathway (as reflected by the conversion of exogenous corticosterone to aldosterone in the presence of cyanoketone) were significantly (P < 0·01) inhibited by lanthanum, nifedipine and by reducing the extracellular calcium concentration. However, with dbcAMP stimulation, none of these manipulations modified pregnenolone production. Late pathway activation by dbcAMP was inhibited by lanthanum and a reduction in extracellular calcium, but not by nifedipine. These observations suggest that: (1) the extracellular calcium dependency of dbcAMP-, angiotensin II- and potassium-stimulated aldosterone secretion reflects a need for calcium influx; (2) with dbcAMP stimulation, activation of the late pathway is dependent on calcium influx by a calcium channel-independent mechanism, whereas activation of the early pathway is not dependent on extracellular calcium or calcium influx and (3) activation of both the early and late pathway by angiotensin II and potassium is dependent on calcium influx by a calcium channel-dependent mechanism. Therefore, we conclude that the mechanism of activation of the early aldosterone biosynthetic pathway by dbcAMP is different from angiotensin II or potassium and early pathway activation is distinct from that of late pathway activation with dbcAMP stimulation. J. Endocr. (1986) 110, 315–325

The contractile action of platelet-activating factor on gallbladder smooth muscle

2000 ◽  
Vol 279 (1) ◽  
pp. G67-G72 ◽  
Author(s):  
Henry P. Parkman ◽  
Arlene N. James ◽  
James P. Ryan
Keyword(s):  
Pertussis Toxin ◽  
Contractile Response ◽  
Calcium Influx ◽  
Platelet Activating Factor ◽  
Extracellular Calcium ◽  
Motor Dysfunction ◽  
Gallbladder Contraction ◽  
Voltage Dependent ◽  
Voltage Dependent Calcium Channels

Platelet-activating factor (PAF) may be a mediator of some sequelae of cholecystitis, a disorder with gallbladder motor dysfunction. The aims of this study were to determine the effect and mechanism of PAF on gallbladder muscle. Exogenous administration of PAF-16 or PAF-18 caused dose-dependent contractions of gallbladder muscle strips in vitro with threshold doses of 1 ng/ml and 10 ng/ml, respectively. The PAF-induced contractions were not significantly reduced by TTX, atropine, or hexamethonium but were significantly inhibited with the PAF receptor antagonists ginkolide B and CV-3988. The PAF-induced contraction was reduced by indomethacin. Preventing influx of extracellular calcium with a calcium-free solution nearly abolished the PAF contractile response. Nifedipine inhibited the PAF contractile response, whereas ryanodine had no effect. Pertussis toxin reduced the PAF contractile response. In conclusion, PAF causes gallbladder contraction through specific PAF receptors on gallbladder muscle. These PAF receptors appear to be linked to a prostaglandin-mediated mechanism and to pertussis toxin-sensitive G proteins. The contractile response is largely mediated through the utilization of extracellular calcium influx through voltage-dependent calcium channels.

Sign in / Sign up

Export Citation Format

Share Document