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PubMed1987

The effects of ionophores on steroidogenesis and morphology of avian granulosa cells.

Granulosa cells, isolated by collagenase digestion from the mature ovarian follicle of laying hens, were incubated in the presence of two ionophores, lasalocid (X537A) and ionomycin, to determine their effects on basal and stimulated steroidogenesis, as well as their effects on various cell parameters including DNA, RNA, and protein synthesis. Both ionophores caused a dose-dependent inhibition of agonist-promoted progesterone production and, in the presence of calcium, a small but significant increase in basal output of progesterone. Whereas the conversion of pregnenolone to progesterone was unaffected by the ionophores, the activity of cholesterol side-chain cleavage enzyme was inhibited in a dose-related manner. Both ionophores decreased cellular levels of ATP and inhibited the incorporation of radioactively-labeled precursors into DNA, RNA, and proteins. Morphologically, ionophore-treated cells showed swelling of the rough endoplasmic reticulum. Similar morphological changes were also observed in cells treated with oligomycin, a known metabolic inhibitor. These results suggest that the ionophores lasalocid and ionomycin impair release of energy and thereby exert the principal cause of the inhibited steroidogenic response by granulosa cells to a variety of agonists.

Animals↗
PubMed1994

Isolation and characterization of membrane potential changes associated with release of calcium from intracellular stores in rat thymic lymphocytes.

Membrane potential changes accompanying Ca2+ influx stimulated by release of Ca2+ from intracellular stores (store-regulated Ca2+ uptake) were monitored in BAPTA-loaded rat thymic lymphocytes using the fluorescent indicator bis(1,3-diethylthiobarbituric acid)trimethine oxonol. Depletion of [Ca2+]i stores by the application of thapsigargin, ionomycin or cyclopiazonic acid induced a depolarization which was (i) dependent upon BAPTA-loading, (ii) dependent upon extracellular Ca2+, (iii) independent of extracellular Na+ and (iv) abolished by 5 mM extracellular Ni2+. This depolarization was followed by a charybdotoxin-sensitive repolarization and subsequent hyperpolarization to values approximating the K+ equilibrium potential, consistent with secondary activation of a K+ conductance. These membrane potential changes temporally correlated with Ca2+ influx from the extracellular medium as measured fluorimetrically with indo-1. The divalent cation permeability sequence was investigated by monitoring the magnitude of the depolarization observed following the addition of 4 mM Ca2+, Mn2+, Ba2+ or Sr2+ to cells pretreated with doses of thapsigargin or ionomycin known to activate the store-regulated calcium uptake pathway. On the basis of these experiments, we conclude that the store-regulated Ca2+ uptake pathway has the following permeability sequence: Ca2+ > Mn2+ >> Ba2+, Sr2+ with Mn2+ displaying significant permeability relative to Ca2+. This pathway is distinguishable from other divalent cation uptake pathways reported in other cells types on the basis of its activation by thapsigargin and its high Mn2+ permeability.

Animals↗
PubMed1990

Biphasic rises in cytosolic free Ca2+ in association with activation of K+ and Cl- conductance during the regulatory volume decrease in cultured human epithelial cells.

During exposure to a hypotonic solution (55% osmolarity), cultured human epithelial (Intestine 407) cells exhibit a regulatory volume decrease after osmotic swelling. This process is known to involve parallel activation of volume-regulatory K+ and Cl- conductances. Biphasic increase in the cytosolic free Ca2+ concentration ([Ca2+]i) were observed by microspectrofluorometry, in fura-2-loaded cells upon hypotonic stress. Electrophysiological studies with Ca2(+)-selective and conventional microelectrodes indicated that a biphasic [Ca2+]i increase was associated with a biphasic hyperpolarization, whereas an interposing [Ca2+]i decrease coincided with a transient depolarization. A Ca2+ ionophore, ionomycin, produced a sustained Ca2+ increase and a prolonged hyperpolarization which was sensitive to the K+ channel blocker, quinine. A subsequent hypotonic challenge gave rise to a depolarization, which was sensitive to a stilbene-derivative Cl- channel blocker, without inducing further changes in [Ca2+]i. Normal cell volume regulation in a hypo-osmotic medium could take place even in the presence of ionomycin. It is concluded that a biphasic [Ca2+]i increase is closely associated with activation of the volume-regulatory K+ conductance, and that the interposing [Ca2+]i decrease is neither a causative factor for activation of the volume-regulatory Cl- conductance nor a prerequisite for regulatory volume decrease in epithelial cells exposed to a hypotonic solution.

Biological Transport↗
PubMed1991

A comparison of serum-free media for the support of in vitro mitogen-induced blastogenic expansion of cytolytic lymphocytes.

The high cost and potential dangers of including human AB serum in incubation media used to expand lymphocyte populations in vitro for adoptive immunotherapy have stimulated efforts to develop defined media which can support both the expansion and induction of lymphocytes with tumor cytolytic activity in the absence of serum. Lymphocyte proliferation following exposure to either PHA or the combination of phorbol 12,13-dibutyrate (PDBu) and the calcium ionophore, ionomycin, was evaluated. Although the media tested, X-Vivo 10, HB-104, AIM V, and HL-1, supported the generation of comparable levels of LAK activity after 3-5 days incubation with 10(3) U human recombinant interleukin-2 (rIL-2)/ml, there were striking differences in the ability of each medium to support mitogenically stimulated lymphocytes in the absence of serum, with cells in AIM V and X-Vivo 10 showing the highest levels of DNA synthesis. In long-term cultures (17 days) of blood MNC stimulated by PDBu and ionomycin, X-Vivo 10 and HB-104 yielded the greatest numbers of cells. The addition of 2% AB serum greatly enhanced the ability of each medium to support cell proliferation to equivalent maximum levels. The results indicate that while all four serum-free media were suitable for lymphocyte culture and support the development of LAK activity, they differ in their capacity to support expansion of lymphocyte populations in response to polyclonal mitogenic activation. This latter characteristic should be considered before choosing a particular serum-free formulation as its constituents may affect mechanistic interpretations regarding signal transduction events.

Blood↗
PubMed1995

Activation of the basolateral Cl- conductance by cAMP in rabbit renal proximal tubule S3 segments.

The regulatory mechanism of basolateral Cl- conductance in rabbit renal proximal tubule S3 segments was investigated with conventional and Cl- sensitive microelectrodes. After the basolateral Cl-/HCO3- exchanger was blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS) we increased the bath K+ concentration from 5 mmol/l to 20 mmol/l, which depolarized the cells and thereby increased intracellular Cl- activity ([Cl-]i). This [Cl-]i response was enhanced by +63% in the presence of forskolin (20 mumol/l), by +40% in the presence of dibutyryl adenosine 3',5'-cyclic monophosphate (db-cAMP) (1 mmol/l) and by +44% in the presence of parathyroid hormone (PTH, 10 nmol/l), whereas it was inhibited by a Cl- channel blocker, indanyl-oxyacetic acid (IAA-94, 0.3 mmol/l). In addition, forskolin, PTH and chlorophenylthio-cAMP enhanced the electrogenic response to removal of bath Cl- after the blockade of K+ conductance, and this activation was also sensitive to IAA-94. On the other hand, 2 mumol/l ionomycin and 0.5 mumol/l phorbol myristate failed to activate the [Cl-]i response to elevation of bath K+ concentration and the electrogenic response to Cl- removal, and ionomycin had no effect even in the absence of DIDS. These results indicate that this basolateral Cl- conductance can be activated by cAMP, while neither the increase in cytosolic Ca2+ nor the activation of protein kinase C has direct effects on this conductance.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1993

Ca2+ release in cultured rat epididymal cells during hypoosmotic swelling.

Microfluorimetric studies were carried out to investigate the effects of hypoosmotic swelling on intracellular Ca2+ concentration ([Ca2+]i) in single rat epididymal cells. In Ca(2+)-free solution containing 50 mumols/l ethylenebis(oxonitrilo)tetraacetate (EGTA) hypoosmotic swelling (-160 mosmol/l) induced a transient rise in [Ca2+]i which was either monophasic, biphasic or oscillatory. The [Ca2+]i responses to repeated hypoosmotic stimulations followed a decremental pattern. However, if 2.5 mmol/l Ca2+ was admitted during the recovery period between successive stimulations, the second and the third [Ca2+]i responses were slightly greater than the first. Increasing the change in osmolarity from -14 +/- 1.0 to -154 +/- 1.5 mosmol/l increased the rise in [Ca2+]i but reduced the [Ca2+]i response to subsequent ionomycin stimulation (4 mumols/l). The swelling- and the ionomycin-induced rises in [Ca2+]i followed a reciprocal pattern. It was suggested that intracellular Ca2+ release in response to cell swelling in the epididymal epithelium might play a role in cell volume regulation and the control of epididymal fluid osmolarity.

Animals↗
PubMed1994

Histamine modulates three types of K+ current in a human intestinal epithelial cell line.

K+ conductance species in a human intestinal epithelial cell line (Intestine 407) were studied in connection with their sensitivities to an intestinal secretagogue, histamine, using the tight-seal whole-cell patch-clamp technique. Applications of positive command pulses rapidly induced outward K+ currents. The conductance became progressively larger with increasing command voltages, exhibiting an outwardly rectifying current voltage relation. Inward K+ currents were also rapidly activated upon applications of hyperpolarizing pulses at potentials negative to the equilibrium potential of K+ (EK), and the conductance inwardly rectified. Application of a Ca2+ ionophore, ionomycin, brought about activation of additional K+ currents. An inhibitor of protein kinase C, polymyxin B, did not affect the ionomycin-induced response. Histamine (10-200 microM) also activated a similar K+ current which was abolished by cytosolic Ca2+ chelation. Under conditions where Ca2+ mobilization was minimized, histamine was found to significantly augment inwardly rectifying K+, but suppress outwardly rectifying K+, currents. Polymyxin B blocked these effects of histamine. An activator of protein kinase C, 1-oleoyl-2-acetylglycerol, mimicked the histamine effects. It is concluded that the intestinal epithelial cell has three distinct types of K+ conductance and that histamine modulates not only Ca(2+)-activated K+ conductance via Ca2+ mobilization, but also inward- and outward-rectifier K+ conductances via activation of protein kinase C.

Calcium↗
PubMed1993

Differential effects of tamoxifen and I- on three distinguishable chloride currents activated in T84 intestinal cells.

The whole-cell mode of the patch-clamp technique has been used to monitor ionic currents in T84 colonic carcinoma cells. The cells were stimulated by either a cAMP cocktail, ionomycin or hypotonicity. Sizeable currents with distinct kinetics were observed after the stimulation with the different agonists. These kinetically distinct Cl- currents also presented a differential sensitivity to the anti-oestrogen Tamoxifen and to the halide I-. Tamoxifen only inhibits the volume activated Cl- current without affecting the other two. Substitution of extracellular Cl- by I- shifted the reversal potential towards more negative values both in the hypotonicity and ionomycin activated Cl- currents. The cAMP activated current responded to the Cl- substitution by I- with a blockade of both outward and inward currents, in addition to the displacement of the zero current level towards positive values. Thus, the use of these two simple tools, I- and tamoxifen, allows the distinction of Cl- channels in epithelial cells.

Carcinoma↗
PubMed1993

Increase in cytosolic Ca2+ regulates exocytosis and Cl- conductance in HT29 cells.

Increases of cytosolic Ca2+, as occur with agonists such as ATP, neurotensin (NT), hypotonic cell swelling and ionomycin, enhance the membrane conductance (GM) and hence the input conductance (GI) of HT29 cells. In the present study we have examined whether these increases in GM are paralleled by exocytosis. To this end the membrane capacitance (CM) of HT29 cells was measured by patch clamp techniques. Two methods to monitor CM were used: a direct method (DM) and a phase tracking method (PTM). With the DM the following results were obtained. NT (10(-8) mol/l, n = 9) increased GM and CM significantly from 2.4 +/- 0.3 nS and 23.5 +/- 3 pF to 32 +/- 8 nS and 27.3 +/- 3.1 pF respectively. ATP (10(-4) mol/l, n = 29) had a very similar effect. GM and CM were increased from 5.7 +/- 1 nS and 36 +/- 4.4 pF to 111 +/- 21 nS and 44 +/- 5.4 pF respectively. Hypotonic cell swelling (160 mosmol/l, n = 18) had a comparable effect: GM and CM were increased from 4.9 +/- 1 nS and 30 +/- 4.1 pF to 46 +/- 10 nS and 37 +/- 4.9 pF respectively. Ionomycin (10(-7) mol/l, n = 4) gave similar results. With the PTM it was possible to monitor the rapid changes in GM and CM, as they were induced by ATP (n = 42) and NT (n = 29), with high time resolution.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1988

Bile acids increase cellular free calcium in cultured kidney cells (LLC-PK).

Suspensions of LLC-PK1 cells were used to determine the effect of bile acids on the cellular homeostasis of inorganic ions. It is determined that bile acids alter cellular free calcium (Cai) levels in LLC-PK1 cells. A series of bile acids were compared and found to produce increases in Cai in the order: lithocholate sulfate (LCS) greater than deoxycholate greater than chenodeoxycholate greater than lithocholate glucuronide greater than cholate. LCS (300 microM) produces changes in Cai (measured using Fura-2) qualitatively similar to those produced by 1 microM ionomycin, except that only ionomycin is able to release calcium from intracellular stores. The effect on Cai is roughly proportional to LCS concentration between 50 and 300 microM. The presence of 40 mM Na in the extracellular medium reduces the LCS-induced rise in Cai to 20% of that observed in the absence of Na. This effect is specific for Na versus 150 mM extracellular K, Li, or TMA. The effect is not dependent on the Na gradient across the membrane. At concentrations of LCS which induce changes in Cai, no significant effect of LCS is observed on either cellular Na or K levels, or intracellular pH.

Animals↗
PubMed1988

Activation of K+ and Cl- channels by Ca2+ and cyclic AMP in dissociated kidney epithelial (MDCK) cells.

In dissociated MDCK cells, activators of the cyclic AMP system cause depolarization detectable by changes in fluorescence of the membrane potential sensitive dye bisoxonol. Addition of forskolin (60 microM), vasopressin (2 microM), 8-bromo-cyclic AMP (0.5 mM) or 1-epinephrine (10 microM) depolarized the cells substantially in low Cl- (5 mM) but had little effect in high Cl- (140 mM) solution. These results are consistent with cyclic AMP activation of Cl- channels. The Ca2+-ionophore ionomycin (1 microM) produced a rapid hyperpolarization in low and high Cl- solutions, consistent with K+ channel opening. Using a clonal subline, MDCK-14, the magnitude of the ionomycin hyperpolarization was roughly proportional to the concomitant rise in [Ca2+]i as measured with the intracellular Ca2+ probe indo-I. Both l-epinephrine and isoproterenol appeared to activate the Cl- channels. However only l-epinephrine produced a [Ca2+]i rise and a transient hyperpolarization (due to K+ channel opening), which preceded the depolarization due to Cl- channel opening. The l-epinephrine-induced [Ca2+]i response of the heterogeneous MDCK cell population but not of the clonal subline MDCK-14 was inhibited by removal of extracellular Ca2+. In the latter only the slow secondary phase of the [Ca2+]i rise was affected by Ca2+ removal. It is concluded that l-epinephrine activates K+ and Cl- channels in a sequential manner in MDCK cells by Ca2+ and cAMP signals, presumably via alpha- and beta-adrenergic receptors located on the same cell.

Animals↗
PubMed1991

Sodium inhibits hormone release and stimulates calcium efflux from isolated nerve endings of the rat neurohypophysis.

1. We studied the effects of extracellular sodium on the secretion of vasopressin (VP) and oxytocin (OT) and the efflux of 45Ca from isolated, perfused nerve endings of the rat neurohypophysis (neurosecretosomes). 2. Upon removal of sodium from the perfusing medium, basal release of VP and OT increased by 3.95 +/- 0.23- and 3.71 +/- 0.22-fold, respectively, followed by a decline to about double the levels in normal (150 mM) sodium (P less than or equal to 0.1). 3. Compared to neurosecretosomes perfused in normal (150 mM) sodium, omission of sodium from the medium augmented ionomycin-induced VP and OT secretion by 66 +/- 5- and 20 +/- 3-fold, respectively, and A23187-induced secretion was increased 1.3 +/- 0.4- and 1.3 +/- 0.1-fold (P less than or equal to 0.01 for both ionophores). 4. The inhibition of ionomycin-induced secretion by sodium was concentration dependent (P less than or equal to 0.01 for sodium greater than or equal to 5 mM); the IC50 was about 10 mM sodium for both hormones, and the Hill slope was close to -1. 5. The rate of 45Ca efflux from neurosecretosomes showed 2.7 +/- 0.1-fold stimulation upon increasing sodium from 4.5 to 150 mM (P less than or equal to 0.01). 6. Our results suggest that sodium inhibits basal and stimulated secretion at the nerve terminal, possibly by reducing intraterminal calcium through sodium/calcium exchange.

Animals↗
PubMed1988

In vitro effects of omega-3 fatty acids on neutrophil intracellular calcium homeostasis and receptor expression for FMLP and LTB4.

Diets enriched in omega-3 fatty acids exert antiinflammatory properties by suppressing some neutrophil (PMN) functions. Changes in cytosolic Ca2+ concentration, [Ca2+]i, are important for PMN activation and are in part regulated by membrane Ca2+ ATPases. Since membrane proteins are influenced by their lipid environment, we investigated the in vitro effects of the omega-3 fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the [Ca2+]i of PMNs in response to f-Met-Leu-Phe (FMLP), leukotriene B4 (LTB4), and ionomycin. The resting [Ca2+]i of PMNs (in high Ca2+ environment) was increased after pretreatment (37 degrees C, 2 h) with DHA, but not with EPA, or the other fatty acids, oleic acid (OA), or linolenic acid (LA). The stimulated [Ca2+]i by either FMLP or LTB4 was suppressed in a high Ca2+ environment after pretreatment with either EPA or DHA but not with OA or LA. The stimulated [Ca2+]i rise by ionomycin was augmented after pretreatment with DHA but not with EPA, OA, or LA. Pretreatment of PMNs with either EPA or DHA reduced the receptor expression for both FMLP and LTB4. Since omega-3 fatty acids inhibit the expression of receptors for two activators of PMNs, FMLP and LTB4, as well as the [Ca2+]i rise in response to those two stimuli, we propose that the antiinflammatory properties of EPA and DHA may be attributed, at least in part, to alteration in membrane activation of phagocytes.

Adult↗
PubMed1994

Ability of low-dose cyclophosphamide to overcome metastasis-induced immunosuppression.

BACKGROUND: Lymphocytes obtained from tumor-draining lymph nodes (DLN) can have potent in vivo antitumor activity after in vitro activation with bryostatin 1 and ionomycin. However, the presence of visceral metastases in the donor can inhibit the effectiveness of such lymphocytes. In the present study, we tested the ability of low-dose cyclophosphamide to overcome metastasis-induced immunosuppression in a murine model. METHODS: Mice were injected with MCA-105 sarcoma cells in the footpad alone or in the footpad and the tail vein to establish lung metastases. Cyclophosphamide was given i.p. 1 day before harvesting the draining popliteal lymph nodes. For all donor groups, DLN cells were activated with 5 nM bryostatin 1 and 1 microM ionomycin and cultured for 7 days in 20 U/ml IL-2. Activated DLN cells were then adoptively transferred to syngeneic mice with 3-day lung metastases. RESULTS: The adoptive transfer of DLN cells from mice with footpad tumors only significantly reduced the number of lung metastases compared to untreated mice. However, activated DLN cells obtained from mice with both footpad and lung tumors were significantly less effective. Treatment of similar donor mice with 10 mg/kg cyclophosphamide significantly improved the anti-tumor activity of adoptively transferred cells. This dose of cyclophosphamide did not reduce the number of cells obtained from each lymph node or the expansion of cell numbers in vitro. CONCLUSIONS: These results suggest that the administration of low-dose cyclophosphamide prior to harvesting DLN cells may improve the success of adoptive immunotherapy in cancer patients.

Animals↗
PubMed1996

Mycoplasma orale infection affects K+ and Cl- currents in the HSG salivary gland cell line.

The relations between K+ channel and Cl- channel currents and mycoplasma infection status were studied longitudinally in HSG cells, a human submandibular gland cell line. The K+ channel currents were disrupted by the occurrence of mycoplasma infection: muscarinic activation of K+ channels and K+ channel expression as estimated by ionomycin- or hypotonically induced K+ current responses were all decreased. Similar decreases in ionomycin- and hypotonically induced responses were observed for Cl- channels, but only the latter decrease was statistically significant. Also, Cl- currents could be elicited more frequently than K+ currents (63% of cases versus 0%) in infected cells when tested by exposure to hypotonic media, indicating that mycoplasma infection affects K+ channels relatively more than Cl- channels. These changes occurred in the originally infected cells, were ameliorated when the infection was cleared with sparfloxacin, and recurred when the cells were reinfected. Such changes would be expected to result in hyposecretion of salivary fluid if they occurred in vivo.

Antitubercular Agents↗
PubMed1998

Purinergic receptor-induced changes in paracellular resistance across cultures of human cervical cells are mediated by two distinct cytosolic calcium-related mechanisms.

In human cervical (CaSki) cells, extracellular adenosine triphosphate (ATP) induces an acute decrease in the resistance of the lateral intercellular space (RLIS), phase I response, followed by an increase in tight junctional resistance (RTJ), phase II response. ATP also stimulates release of calcium from intracellular stores, followed by augmented calcium influx, and both effects have similar sensitivities to ATP (EC50 of 6 microM). The objective of the study was to determine the degree to which the changes in [Ca2+]i mediate the responses to ATP. 1,2-bis (2-aminophenoxy) ethane-N,N,N1,N1-tetraacetic acid (BAPTA) abrogated calcium mobilization and phase I response; in contrast, nifedipine and verapamil inhibited calcium influx and attenuated phase II response. Barium, La3+, and Mn2+ attenuated phase I response and attenuated and shortened the ionomycin-induced phase I-like decrease in RLIS, suggesting that store depletion-activated calcium entry was inhibited. Barium and La3+ also inhibited the ATP-induced phase II response, but Mn2+ had no effect on phase II response, and in the presence of low extracellular calcium it partly restored the increase in RTJ. KCl-induced membrane depolarization stimulated an acute decrease in RLIS and a late increase in RTJ similar to ATP, but only the latter was inhibited by nifedipine. KCl also induced a nifedipine-sensitive calcium influx, suggesting that acute increases in [Ca2+]i, regardless of mobilization or influx, mediate phase I response. Phase II-like increases in RTJ could be induced by treatment with diC8, and were not affected by nifedipine. Biphasic, ATP-like changes in RTE could be induced by treating the cells with ionomycin plus diC8. We conclude that calcium mobilization mediates the early decrease in RLIS, and calcium influx via calcium channels activates protein kinase C and mediates the late increase in RTJ.

Adenosine Triphosphate↗
PubMed1999

Halothane decreases calcium sensitivity of rat aortic smooth muscle.

PURPOSE: To examine the effect of halothane on the cytosolic Ca2+ concentration ([Ca2+]i)-tension relationship of rat aortic smooth muscle. METHODS: Rat aortic rings without endothelia were loaded with the fluorescent Ca2+ indicator, Fura PE3-AM, and then mounted in organ baths. The changes in isometric tension and [Ca2+]i were measured simultaneously. In one series ionomycin (10 nM-3 microM) was added to normal Krebs' solution cumulatively in the absence and presence of halothane (1.5%, 3%). In the other series, CaCl2 (0.3-3 mM) was added to Ca2+-free Krebs' solution including high KCl (50 mM), phenylephrine (100 nM) or prostaglandin F2alpha (PGF2alpha, 1-3 microM) in the absence and presence of halothane (1.5%, 3%). The linear part of [Ca2+]i-tension relationship was analyzed by a linear regression. RESULTS: Halothane, 1.5%, had no effect on the normal [Ca2+]i-tension relationship obtained with the calcium ionophore, ionomycin (10 nM-3 microM), but halothane 3% decreased the slope of the relationship (0.239 +/- 0.037 for control and 0.110 +/- 0.010 for halothane 3%, P < 0.05). Halothane, 1.5% and 3%, did not change the [Ca2+]i-tension relationship obtained with CaCl2 (0.3-3 mM) in the presence of high KCl (50 mM) or phenylephrine (100 nM). In contrast, halothane, 3%, inhibited the intercept of [Ca2+]i-tension relationship obtained with CaCl2 (0.3-3 mM) in the presence of prostaglandin F2alpha (PGF2alpha, 1-3 microM) (45.708 +/- 4.233 for control and 26.997 +/- 2.522 for halothane 3%, P < 0.01). CONCLUSION: Halothane decreases the Ca2+ sensitivity and that in the presence of PGF2.

Anesthetics, Inhalation↗
PubMed1996

Regulation of cell volume by beta2-adrenergic stimulation in rat fetal distal lung epithelial cells.

Cell-volume changes induced by terbutaline (a specific beta2-agonist) were studied morphometrically in rat fetal distal lung epithelium (FDLE) cells. Cell-volume changes qualitatively differed with the concentration of terbutaline. Terbutaline of 10(-10)-10(-8) M induced transient cell swelling. Terbutaline of 10(-7) M induced transient cell swelling followed by slow cell shrinkage. Terbutaline of 10(-6)-10(-5) M induced rapid cell shrinkage followed by slow cell shrinkage. Terbutaline of 10(-3) M induced transient cell shrinkage; then cell volume oscillated during stimulation. Benzamil of 10(-6) M suppressed the cell swelling induced by 10(-10)-10(-8) M terbutaline and quinine of 10(-3) M inhibited the cell shrinkage induced by 10(-6)-10(-5) M terbutaline. These results suggest that cell swelling would be induced by NaCl influx and the cell shrinkage is by KCl efflux. Dibutyryl cyclic AMP (DBcAMP) also induced similar cell-volume changes over a wide range of concentrations (10(-9)-10(-3) M): a low concentration induced transient cell swelling; a high concentration, rapid and slow cell shrinkage. Forskolin (10(-4) M), like terbutaline (10(-5) M), induced rapid cell shrinkage followed by slow cell shrinkage, and this decrease in the cell volume was enhanced by the presence of benzamil. On the other hand, cell shrinkage was induced by ionomycin (even low concentration; 3 x 10(-10) M ionomycin), and after that cell volume remained at a plateau level. Removal of extracellular Ca2+ abolished the cell swelling caused by terbutaline of 10(-10)-10(-8) M. With removal of extracellular Ca2+, the initial, rapid cell shrinkage induced by 10(-5) M terbutaline became transient, but we still detected slow cell shrinkage similar to that in the presence of extracellular Ca2+. Overall, at low concentrations (10(-10)-10(-8) M), terbutaline induced benzamil-sensitive cell swelling in FDLE cells, which was cAMP- and Ca2+-dependent; high concentrations (> or =10(-6)) induced quinine-sensitive rapid cell shrinkage, which was Ca2+-dependent; high concentrations (> or = 10(-7)) induced slow cell shrinkage, which was cAMP-dependent. These findings suggest that terbutaline regulates cell volume in FDLE cells by cytosolic cAMP and Ca2+ through activation of Na+ and K+ channels.

Adrenergic beta-Agonists↗