A comparison of antigen-induced and calcium ionophore A23187 induced contraction of isolated guinea pig trachea

1981 ◽  
Vol 59 (10) ◽  
pp. 1031-1038 ◽  
Author(s):  
John F. Burka ◽  
Nigel A. M. Paterson
Keyword(s):  
Guinea Pig ◽  
Calcium Ionophore ◽  
Arachidonic Acid Metabolism ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Ionophore A23187 ◽  
Lipoxygenase Inhibitor ◽  
Lipoxygenase Pathway ◽  
Histamine Secretion ◽  
Other Hand

Ovalbumin (OA) and the calcium ionophore A23187 induced a dose-dependent contraction of guinea pig tracheal strips. The OA-induced contraction (of sensitized trachea) consisted of an initial peak contraction, maximal between 5 and 10 min, followed by a very gradual decline from the peak. On the other hand, A23187 induced a sustained contraction of the trachea with a more gradual onset. Both antigen- and A23187-induced contractions required the presence of extracellular calcium. The response was not reduced by delaying (up to 10 min) the addition of calcium, suggesting that the mechanism of antigen-induced contraction differs from that of antigen-induced histamine secretion from rat mast cells and human basophils. The 1st min of the OA-induced contraction was inhibited significantly by mepyramine (10−5 M) suggesting that histamine contributed to the contraction at this time point. In contrast, A23187-induced contraction was unaffected by mepyramine. On the other hand, both the A23187-induced contraction and the prolonged phase of the OA-induced contraction were enhanced by indomethacin, a cyclooxygenase inhibitor, and inhibited by phenidone, a cyclooxygenase–lipoxygenase inhibitor. This suggests that a product of the lipoxygenase pathway of arachidonic acid metabolism contributes to OA- and A23187-induced contraction of the guinea pig trachea.

Inhibition of antigen and calcium ionophore A23187 induced contractions of guinea pig airways by isoprenaline and forskolin

1983 ◽  
Vol 61 (6) ◽  
pp. 581-589 ◽  
Author(s):  
John F. Burka
Keyword(s):  
Guinea Pig ◽  
Calcium Ionophore ◽  
Arachidonic Acid Metabolism ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Inhibitory Effects ◽  
Lipoxygenase Pathway ◽  
Low Concentrations ◽  
Peak Phase ◽  
Initial Peak

Isoprenaline and forskolin both inhibit contractions induced by antigen or by the calcium ionophore A23187 of guinea pig tracheal spirals and parenchymal strips. Antigen-induced airway contraction is considerably more sensitive to the inhibitory effects of isoprenaline than is A23187-induced contraction. In contrast, forskolin is equiactive as an inhibitor of antigenic and ionophoric contractions. Forskolin is a more effective inhibitor of the prolonged phase of antigen-induced tracheal contraction than of the initial peak phase, which may suggest selectivity for the lipoxygenase pathway of arachidonic acid metabolism. Isoprenaline inhibits the mechanisms of the primary peak phase and of the prolonged phase equally. Although there were little, if any, differences between normal and sensitized tissues in the modulation of A23187-induced contractions of parenchyma, distinct differences were observed in trachea. Low concentrations (10−8–10−7 M) of isoprenaline and forskolin enhanced A23187-induced contraction of sensitized, but not normal trachea. Higher concentrations were inhibitory. The results demonstrate that sensitization affects the modulation by isoprenaline and forskolin of A23187-indueed contraction of guinea pig trachea.

Inhibitory effects of calcium ionophore pretreatment of porcine oocytes on polyspermic fertilization

Zygote ◽  
2006 ◽  
Vol 14 (1) ◽  
pp. 17-22 ◽  
Author(s):  
T. Hayashi ◽  
H. Sato ◽  
H. Iwata ◽  
T. Kuwayama ◽  
Y. Monji
Keyword(s):  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Ionophore A23187 ◽  
Inhibitory Effects ◽  
High Concentration ◽  
Maturation Period ◽  
Low Concentration ◽  
Other Hand

The present study examined the inhibitory effects of various pretreatment concentrations (0–100 μM) of the calcium ionophore A23187 on polyspermic fertilization and then examined the effect of the maturation period and the time between calcium ionophore treatment and fertilization on the inhibitory effect of calcium ionophore on polyspermic fertilization. In experiment 1, a high concentration of calcium ionophore (100 μM) increased the rate of activated oocytes, but the rate of fertilization declined. On the other hand, when oocytes were treated with a low concentration of calcium ionophore (10 μM), monospermic fertilization was significantly increased (10 μM; 31.3%) (p < 0.05). In experiment 2, oocytes were cultured for various times (0, 0.5, 3, 6 h) after calcium ionophore treatment (10 μM) before fertilization. The highest rate of monospermic fertilization was detected in the oocytes cultured for 6 h after calcium ionophore treatment before fertilization. In experiments 3 and 4, we examined the effect of the maturation period (40 h or 44 h) on the rate of fertilization and blastulation of oocytes pretreated with calcium ionophore. The treatment of oocytes with calcium ionophore significantly decreased the rate of polyspermic fertilization regardless of the maturation period (44 h: with calcium ionophore 26.25% vs without 78.8%; 40 h: with calcium ionophore 37.5% vs without 77.5%); however, calcium ionophore treatment increased the rates of monospermic fertilization and blastulation of the oocytes matured for 44 h, but not those matured for 40 h. In conclusion, activation with a low concentration of calcium ionophore (10 μM) and a further 6 h of culture before fertilization improved the rate of monospermic fertilization and blastulation.

scholarly journals Leukotriene generation by eosinophils.

1982 ◽  
Vol 155 (2) ◽  
pp. 390-402 ◽  
Author(s):  
A Jörg ◽  
W R Henderson ◽  
R C Murphy ◽  
S J Klebanoff
Keyword(s):  
Arachidonic Acid ◽  
Calcium Ionophore ◽  
Leukotriene B4 ◽  
Arachidonic Acid Metabolism ◽  
Calcium Ionophore A23187 ◽  
Eicosatetraenoic Acid ◽  
Gas Chromatography Mass Spectrometry ◽  
Ionophore A23187 ◽  
Lipoxygenase Pathway ◽  
Leukotriene D4

Horse eosinophils purified to greater than 98% generated slow reacting substance (SRS) when incubated with the calcium ionophore A23187. On a per cell basis, eosinophils generated four to five times the SRS produced by similarly treated horse neutrophils. Eosinophil SRS production was inhibited by 5,8,11,14-eicosatetraynoic acid and augmented by indomethacin and arachidonic acid, suggesting that it was a product(s) of the lipoxygenase pathway of arachidonic acid metabolism. Compounds with SRS activity were purified by high-pressure liquid chromatography (HPLC) and identified by ultraviolet spectra, spectral shift on treatment with lipoxygenase, incorporation of [14C]arachidonic acid, gas chromatography-mass spectrometry, and comparison of retention times on HPLC to authentic standards. The eosinophil products characterized were 5-(S), 12-(R)-dihydroxy-6-cis-8, 10-trans-14-cis-eicosatetraenoic acid (leukotriene B4) and its 5-(S), 12-(R)-6-trans and 5-(S), 12-(S)-6-trans isomers, 5-(S)-hydroxy-6-(R)-S-glutathionyl-7,9-trans-11, 14-cis-eicosatetraenoic acid (leukotriene C4) and its 11-trans isomer, and 5-(S)-hydroxy-6-(R)-S-cysteinylglycine-7,9-trans-11,14-cis-eicosatetraenoic acid (leukotriene D4).

scholarly journals Toxoplasma gondii alters eicosanoid release by human mononuclear phagocytes: role of leukotrienes in interferon gamma-induced antitoxoplasma activity.

1994 ◽  
Vol 180 (5) ◽  
pp. 1637-1648 ◽  
Author(s):  
E C Yong ◽  
E Y Chi ◽  
W R Henderson
Keyword(s):  
Arachidonic Acid ◽  
Toxoplasma Gondii ◽  
Calcium Ionophore ◽  
Arachidonic Acid Metabolism ◽  
Calcium Ionophore A23187 ◽  
Mononuclear Phagocytes ◽  
Human Macrophage ◽  
Ionophore A23187 ◽  
Lipoxygenase Inhibitor ◽  
Ifn Gamma

Toxoplasma gondii tachyzoites markedly alter the profile of eicosanoids released by human mononuclear phagocytes. Freshly isolated, 2-h adherent human monocytes release both cyclooxygenase (e.g., thromboxane [TX] B2, prostaglandin [PG] E2) and 5-lipoxygenase (e.g., leukotriene [LT] B4, LTC4) products of arachidonic acid metabolism after stimulation by the calcium ionophore A23187 or ingestion of opsonized zymosan particles or heat-killed T. gondii. However, after incubation with viable T. gondii, normal and chronic granulomatous disease monocytes release only the cyclooxygenase products TXB2 and PGE2 and fail to form LTB4, LTC4, or other 5-lipoxygenase products. Monocytes maintained in culture for 5 d lose this capacity to release TXB2 and PGE2 after incubation with T. gondii. T. gondii significantly inhibit calcium ionophore A23187-induced LTB4 release by monocyte-derived macrophages; heat-killed organisms do not affect this calcium ionophore A23187-induced release of LTB4. T. gondii-induced inhibition of LTB4 release by calcium ionophore A23187-stimulated monocyte-derived macrophage is reversed by interferon (IFN)-gamma treatment of the monolayers. LTB4 induced extensive damage to the cellular membranes and cytoplasmic contents of the organisms as observed by transmission electron microscopy. Exogenous LTB4 (10(-6) M) induced intracellular killing of ingested T. gondii by non-IFN-gamma-treated monocyte-derived macrophages. IFN-gamma-induced antitoxoplasma activity in monocyte-derived macrophages was inhibited by the selective 5-lipoxygenase inhibitor zileuton but not by the cyclooxygenase inhibitor indomethacin. These findings suggest a novel role for 5-lipoxygenase arachidonic acid products in human macrophage IFN-gamma-induced antitoxoplasma activity.

scholarly journals Is a rise in intracellular concentration of free calcium necessary or sufficient for stimulated cytoskeletal-associated actin?

1986 ◽  
Vol 102 (4) ◽  
pp. 1459-1463 ◽  
Author(s):  
R I Sha'afi ◽  
J Shefcyk ◽  
R Yassin ◽  
T F Molski ◽  
M Volpi ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Pertussis Toxin ◽  
Incubation Medium ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Extracellular Calcium ◽  
Intracellular Concentration ◽  
The Other ◽  
Free Calcium ◽  
Ionophore A23187

The addition of the calcium ionophore A23187 to rabbit neutrophils increases the amount of actin associated with the cytoskeleton regardless of the presence or absence of calcium in the incubation medium. In the presence of extracellular calcium, the effect of A23187 is biphasic with respect to concentration. The action of the ionophore is rapid, transient, and is inhibited by pertussis toxin, hyperosmolarity, and quinacrine. On the other hand, the addition of pertussis toxin or hyperosmolarity has small if any, effect on the rise in intracellular calcium produced by A23187. While quinacrine does not affect the fMet-Leu-Phe-induced increase in cytoskeletal actin and the polyphosphoinositide turnover, its addition inhibits completely the stimulated increase in Ca-influx produced by the same stimulus. The results presented here suggest that a rise in the intracellular concentration of free calcium is neither necessary nor sufficient for the stimulated increase in cytoskeletal-associated actin. A possible relationship between the lipid remodeling stimulated by chemoattractants and the increased cytoskeletal actin is discussed.

scholarly journals Cross-regulation of cortisol secretion by adrenocorticotropin and platelet-activating factor in perfused guinea pig adrenals

2007 ◽  
Vol 195 (1) ◽  
pp. 29-38
Author(s):  
Toshio Shimada ◽  
Taeko Hirose ◽  
Itsuro Matsumoto ◽  
Tadaomi Aikawa
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Cortisol Response ◽  
Cortisol Secretion ◽  
Induced Signal ◽  
Dependent Processes

We examined the cross-regulation of signaling between ACTH-and platelet-activating factor (PAF)-mediated steroidogenesis in the perfused guinea pig adrenal gland. Our method of in situ perfusion using an artificial medium can evaluate whether cortisol secretion in response to ACTH and PAF is interactive. Treating adrenal glands with 100 pg/ml ACTH diminished the subsequent cortisol response to 10 nM PAF. By contrast, PAF resulted in subsequent potentiation of ACTH-induced cortisol secretion. A mixture of 50 μM l-α-1-oleoyl-2-acetyl-sn-glycerol (OAG), an activator of protein kinase C (PKC), and 3.3 μM calcium ionophore (A23187), or 10 μM forskolin (FRK) diminished the cortisol response to PAF, whereas that to ACTH was unaffected. Each of PAF, ACTH, or FRK eliminated the cortisol response to OAG plus A23187, whereas that to FRK was unaffected. These data show that the protein kinase A (PKA)-dependent processes activated by ACTH or FRK can interfere with PAF-induced signal transduction at receptor and post-receptor levels. In contrast, PKC-dependent processes activated by PAF promoted ACTH-signaling at receptor and post-receptor level. Cross-regulation between processes activated by PAF receptor–PKC and by ACTH receptor–PKA might function in the multifactorial regulation of adrenocortical steroidogenesis.

The calcium ionophore A23187 stimulates glycoprotein secretion by the guinea pig gallbladder

Hepatology ◽  
1986 ◽  
Vol 6 (4) ◽  
pp. 569-573 ◽  
Author(s):  
Peter F. Malet ◽  
Catherine L. Locke ◽  
Bruce W. Trotman ◽  
Roger D. Soloway
Keyword(s):  
Guinea Pig ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Glycoprotein Secretion

scholarly journals Platelet-activating factor acts on cortisol secretion by perfused guinea-pig adrenals via calcium-/phospholipid-dependent mechanisms

2005 ◽  
Vol 184 (2) ◽  
pp. 381-391 ◽  
Author(s):  
Toshio Shimada ◽  
Taeko Hirose ◽  
Itsuro Matsumoto ◽  
Tadaomi Aikawa
Keyword(s):  
Protein Kinase ◽  
Guinea Pig ◽  
Platelet Activating Factor ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Breakdown Product ◽  
Ionophore A23187 ◽  
Cortisol Secretion ◽  
Cortisol Responses ◽  
Paf Receptor

Bilateral adrenals of the guinea pig were perfused in situ with an artificial medium equilibrated with 95% O2/5% CO2. Platelet-activating factor (PAF) induced biphasic cortisol responses, which reached a maximum at 10 nM PAF and declined at 100 nM. The effect of the PAF receptor antagonists CV-3988 and CV-6209 on PAF-stimulated cortisol secretion was examined. Prior exposure of adrenal glands to 10 μM CV-3988 or a simultaneous incubation with 10 μM CV-6209 abolished the cortisol response to 10 nM PAF. Lyso-PAF (a PAF precursor and breakdown product) did not affect cortisol secretion. Concentrations of 5–12.5 μM 1-(5-isoquinolinesulfonyl)-2-methylpiperazine dihydrochloride (H-7), a protein kinase C (PKC) inhibitor, abolished subsequent cortisol secretion in response to 10 nM PAF. N-[2-(Methylamino)ethyl]-5-isoquinoline sulfonamide dihydrochloride (H-8), a protein kinase A inhibitor, was less effective. A calcium ionophore (A23187) at 3.3 and 10 μM increased cortisol secretion, but the activator of PKC, l-α-1-oleoyl-2-acetyl-sn-3-glycerol (OAG), at 50 μM had no effect. When infused simultaneously, OAG (50 μM) and A23187 (3.3 μM) stimulated cortisol secretion synergistically. The secretory response of cortisol to repeated infusions of adrenocortico-trophin (100 pg/ml) or forskolin (10 μM) was essentially reproducible. By contrast, cortisol secretion in response to repeated infusions of PAF (10 nM) or OAG plus A23187 was not reproducible and the second response was diminished compared with the first. Our findings suggest that PAF plays a role in the regulation of steroidogenesis via a mechanism mediated by the PAF receptor and PKC.

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