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.

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.

Effects of glucocorticoids on prostaglandin formation by human amnion

1990 ◽  
Vol 68 (6) ◽  
pp. 671-676 ◽  
Author(s):  
William Gibb ◽  
Jean-Claude Lavoie
Keyword(s):  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Isolated Cells ◽  
Stimulatory Action ◽  
Human Amnion ◽  
Human Labor ◽  
Epidermal Growth

The human amnion may be an important source of prostaglandins involved in the onset of human labor and therefore it is important to define the factors that regulate their formation in this tissue. In the present study we demonstrate that glucocorticoids inhibit prostaglandin production by freshly isolated amnion cells. The inhibitory action of the glucocorticoids, however, changes to a stimulatory action when the cells are maintained in primary culture for a few days. For both inhibition and stimulation, concentrations of 10−8 M dexamethasone or greater were required to give significant effects, and estradiol and progesterone had no effect on the prostaglandin output of the cells. Epidermal growth factor (EGF), which has previously been found to stimulate prostaglandin output by confluent amnion cells, did not alter prostaglandin output of cells initially placed in culture. Furthermore, the stimulatory action of EGF and dexamethasone appeared additive. The calcium ionophore A23187 stimulated prostaglandin output in freshly isolated cells and accentuated the inhibitory effect of dexamethasone. These studies indicate that prostaglandin formation by human amnion during pregnancy could be regulated by glucocorticoids. These steroids are easily available to the amnion by way of cortisone conversion to Cortisol by the maternal decidua. The results also indicate that amnion is capable of responding to glucocorticoids in both a stimulatory and inhibitory fashion and whether one or both actions are of importance in vivo is a question that is as yet unresolved.Key words: prostaglandins, amnion, fetal membranes, glucocorticoids, labor, pregnancy.

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.

Inhibitory Effects of Etomidate and Ketamine on Endothelium-dependent Relaxation in Canine Pulmonary Artery

2001 ◽  
Vol 94 (4) ◽  
pp. 668-677 ◽  
Author(s):  
Koji Ogawa ◽  
Satoru Tanaka ◽  
Paul A. Murray
Keyword(s):  
Pulmonary Artery ◽  
Calcium Ionophore ◽  
Receptor Activation ◽  
Isometric Tension ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Inhibitory Effects ◽  
Pulmonary Arterial ◽  
Synthase Inhibitor ◽  
Endothelium Dependent Relaxation

Background The authors recently demonstrated that acetylcholine-induced pulmonary vasorelaxation had two primary components, nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). The goal was to investigate the effects of etomidate and ketamine on the NO- and EDHF-mediated components of pulmonary vasorelaxation in response to acetylcholine, bradykinin, and the calcium ionophore, A23187. Methods Canine pulmonary arterial rings with an intact endothelium were suspended in organ chambers for isometric tension recording. The effects of etomidate and ketamine (10(-5) M and 10(-4) M) on vasorelaxation responses to acetylcholine, bradykinin, and A23187 were assessed in phenylephrine-contracted rings. The NO- and EDHF-mediated components of relaxation were assessed using a NO synthase inhibitor (N-nitro-L-arginine methylester [L-NAME]: 10(-4) M) and a Ca2+-activated potassium channel inhibitor (tetrabutylammonium hydrogen sulfate [TBA]: 10(-3) M) in rings pretreated with a cyclooxygenase inhibitor (ibuprofen: 10(-5) M). Intracellular calcium concentration ([Ca2+]i) was measured in cultured bovine pulmonary artery endothelial cells loaded with acetoxylmethyl ester of fura-2. Results Etomidate and ketamine attenuated pulmonary vasorelaxation in response to acetylcholine and bradykinin, whereas they had no effect on the response to A23187. The relaxant responses to acetylcholine and bradykinin were attenuated by L-NAME or TBA alone and were abolished by combined inhibition in rings pretreated with ibuprofen. Etomidate and ketamine further attenuated both L-NAME-resistant and TBA-resistant relaxation. These anesthetics also inhibited increases in endothelial [Ca2+]i in response to bradykinin, but not A23187. Conclusion These results indicate that etomidate and ketamine attenuated vasorelaxant responses to acetylcholine and bradykinin by inhibiting both NO- and EDHF-mediated components. Moreover, our results suggest that these anesthetics do not directly suppress NO or EDHF activity, but rather inhibit the endothelial [Ca2+]i transient in response to receptor activation.

Singlet oxygen scavengers affect laser-dye impairment of endothelium-dependent responses of brain arterioles

1996 ◽  
Vol 270 (4) ◽  
pp. H1258-H1263 ◽  
Author(s):  
W. I. Rosenblum ◽  
G. H. Nelson
Keyword(s):  
Singlet Oxygen ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Protective Effects ◽  
Laser Dye ◽  
Oxygen Scavengers ◽  
Heat Injury

This study investigates the possible role of singlet oxygen in accounting for the inhibitory effect of laser-dye injury on endothelium-dependent dilations. The combination of helium-neon (HeNe) laser (20-s exposure) and intravascular Evans blue impairs endothelium-dependent dilation of mouse pial arterioles by acetylcholine (ACh), bradykinin (BK), and calcium ionophore A23187. Each has a different endothelium-derived mediator (EDRFACh, EDRFBK, EDRFionophore, respectively). In this study, diameters at a craniotomy site were monitored in vivo with an image splitter-television microscope. The laser-dye injury, as usual, abolished the responses 10 and 30 min after injury, with recovery, complete or partial, at 60 min. Dilations by sodium nitroprusside, an endothelium-independent dilator, were not affected by laser-dye. When the singlet oxygen scavengers L-histidine (10(-3) M) and L-tryptophan (10(-2) M) were added to the suffusate over the site, the responses to ACh at 10 and 30 min were relatively intact, the response to BK was partly protected at 10 min only, and the response to ionophore was still totally impaired at 10 and 30 min. Lysine, a nonscavenging amino acid, had no protective effects with any dilator. We postulate that a heat-induced injury initiates a chain of events resulting in prolonged singlet oxygen generation by the endothelial cell (not by the dye). We postulate further that destruction of EDRFACh by singlet oxygen is responsible for laser-dye inhibition of ACh and that generation of the radical must continue for > or = 30 min. On the other hand, the heat injury itself is probably responsible for the elimination of the response to ionophore. Heat plus singlet oxygen generated by heat-damaged tissue may initially impair the response to BK, but by 30 min only the effects of some other factor, presumably heat injury, account for the impaired response to BK.

Calcium modulates vasopressin effect in rabbit cortical collecting tubule

1987 ◽  
Vol 252 (1) ◽  
pp. F115-F121 ◽  
Author(s):  
M. A. Dillingham ◽  
B. S. Dixon ◽  
R. J. Anderson
Keyword(s):  
Calcium Uptake ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Calcium Activity ◽  
Cellular Calcium ◽  
Collecting Tubules ◽  
Bathing Fluid

The calcium ion has been proposed to be an important mediator of the hydroosmotic response to arginine vasopressin (AVP). We examined the effect of reducing basolateral calcium activity on hydraulic conductivity (Lp) in response to AVP in rabbit cortical collecting tubules (CCT) perfused in vitro. Each tubule served as its own control. Reducing bathing fluid calcium from 0.94 mM to 4.6 microM reduced Lp in each tubule (mean decrease from 146 +/- 13 to 106 +/- 7 cm X s-1 X atm X 10(-7), n = 11, P less than 0.025). To determine whether this inhibitory effect was due to a decrease in cellular calcium uptake, we measured the effect of adding 10(-4) M lanthanum to bathing fluid on AVP-stimulated Lp. Lanthanum decreased Lp (from 109 +/- 13 to 80 +/- 10 cm X s-1 X atm X 10(-7), P less than 0.05) in each tubule. To examine the site at which low peritubular calcium activity regulates AVP action, we measured the effect of decreasing bathing fluid calcium on 8-[p-chlorophenylthio]-adenosine 3',5'-cyclic monophosphate (ClPheS-cAMP)-stimulated Lp (n = 5). Decreasing bathing fluid calcium significantly decreases (P less than 0.025) Lp response to ClPheS-cAMP. Since these results suggest that cellular calcium uptake can exert a post-cAMP effect to modulate AVP action, we examined the effect of the calcium ionophore A23187 (10(-7) M) on AVP- and ClPheS-cAMP-stimulated Lp A23187 reversibly potentiates (25-30%, P less than 0.025) the Lp response to both AVP and ClPheS-cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Inhibitory effect of LY 255283 on the synthesis of leukotriene B4and thromboxane A2in human peripheral blood polymorphonuclear leukocytes and monocytes

1993 ◽  
Vol 2 (6) ◽  
pp. 407-409 ◽  
Author(s):  
M. Ugur ◽  
M. Melli
Keyword(s):  
Receptor Antagonist ◽  
Peripheral Blood ◽  
Polymorphonuclear Leukocytes ◽  
Human Peripheral Blood ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Human Monocytes

LY 255283 [(1-(5-ethyl-2-hydroxy-4-(6-methyl-6-)1H-tetrazol-5-yl)-heptyloxy) phenyl)ethanone], a specific leukotriene B4(LTB4) receptor antagonist, inhibited the production of LTB4in human peripheral blood polymorphonuclear leukocytes (PMNL) and in monocytes activated by calcium ionophore A23187. In human monocytes activated by ionophore it inhibited also the production of thromboxane B2(TXB2). The effect of LY 255283 on 5-lipoxygenase (5-LO) and LTA4hydrolase activities which catalyse the production of LTB4and LTA4has not been studied yet. It is thought that LY 255283 may inhibit the production of LTB4and TXA2by antagonising the effect of ionophore-induced LTB4on 5-lipoxygenase and cyclooxygenase in human peripheral blood PMNL and monocytes.

Heparin inhibits histamine release from canine mast cells

1993 ◽  
Vol 264 (4) ◽  
pp. L387-L390 ◽  
Author(s):  
N. Inase ◽  
R. E. Schreck ◽  
S. C. Lazarus
Keyword(s):  
Mast Cells ◽  
Charge Density ◽  
Histamine Release ◽  
Negative Charge ◽  
Calcium Ionophore ◽  
Inhibitory Effect ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Similar Inhibitory Effect ◽  
Negative Charge Density

To determine the role of heparin in mast cell exocytosis, we studied the effect of heparin on histamine release induced by compound 48/80 or calcium ionophore A23187 in canine mastocytoma cells (BR). Heparin caused concentration-dependent inhibition of compound 48/80-induced histamine release from mast cells (n = 4; P < 0.05) with a mean inhibitory concentration of 0.14 +/- 0.01 U/ml (mean +/- SE). Mean maximal inhibition was 69.3 +/- 2.0%. In contrast, heparin had no effect on calcium ionophore A23187-induced histamine release. Although benzyl alcohol, a preservative of pharmaceutical heparin, had no effect, purified heparin produced a similar inhibitory effect on compound 48/80-induced histamine release (n = 4; P < 0.05). The inhibitory effect of heparin on histamine release was rapid and was eliminated by washing cells. Dextran sulfate, a polysaccharide with negative charge density, produced a similar inhibitory effect on compound 48/80-induced histamine release (n = 4; P < 0.05). We conclude that heparin inhibits compound 48/80-induced exocytosis in mast cells probably by its negative charge density.

Potentiation of pepsinogen secretion from dispersed glands from rat stomach

1983 ◽  
Vol 245 (4) ◽  
pp. G525-G530 ◽  
Author(s):  
J. P. Raufman ◽  
D. K. Kasbekar ◽  
R. T. Jensen ◽  
J. D. Gardner
Keyword(s):  
Vasoactive Intestinal Peptide ◽  
Phosphodiesterase Inhibitor ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
The Other ◽  
Ionophore A23187 ◽  
Rat Stomach ◽  
Gastric Glands ◽  
Cellular Calcium ◽  
Pepsinogen Secretion

In the present study we examined the actions of various agents alone and in combination on pepsinogen secretion from dispersed gastric glands prepared from rat stomach. Potentiation of pepsinogen secretion occurred with secretin or vasoactive intestinal peptide plus carbamylcholine or cholecystokinin. The pattern of action of secretin and vasoactive intestinal peptide could be reproduced by 8-bromo-cAMP, and the pattern of action of carbamylcholine and cholecystokinin could be reproduced by the calcium ionophore A23187. A phosphodiesterase inhibitor, isobutylmethylxanthine, increased pepsinogen secretion, increased the potency but not the efficacy of the action of secretin on pepsinogen secretion, and potentiated the action of carbamylcholine on pepsinogen secretion. These results suggest that, in dispersed gastric glands from rat stomach, secretagogue-induced pepsinogen secretion can be stimulated by two different mechanisms: one mechanism is mediated by cAMP and the other is mediated by changes in cellular calcium. Secretagogues whose actions are mediated by one mechanism potentiate the actions of those secretagogues whose actions are mediated by the other mechanism.

Inhibitory Effect of Fentanyl on Acetylcholine-induced Relaxation in Rat Aorta

2004 ◽  
Vol 101 (1) ◽  
pp. 89-96 ◽  
Author(s):  
Ju-Tae Sohn ◽  
Seong-Ho Ok ◽  
Hee-Jin Kim ◽  
Seon-Hak Moon ◽  
Il-Woo Shin ◽  
...  
Keyword(s):  
Muscarinic Receptor ◽  
Response Curve ◽  
Calcium Ionophore ◽  
Receptor Activation ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Acetylcholine Concentration ◽  
Concentration Response Curve

Background Previous study has shown that fentanyl attenuates acetylcholine-induced vasorelaxation. The goal of the current in vitro study was to identify the muscarinic receptor subtype that is mainly involved in the fentanyl-induced attenuation of endothelium-dependent relaxation elicited by acetylcholine. Methods The effects of fentanyl and muscarinic receptor antagonists on the acetylcholine concentration-response curve were assessed in aortic vascular smooth muscle ring preparations precontracted with phenylephrine. In the rings pretreated independently with pirenzepine, 4-diphenylacetoxyl-N-methylpiperidine methiodide, and naloxone, acetylcholine concentration-response curves were generated in the presence and absence of fentanyl. The effect of fentanyl on the concentration-response curve for calcium ionophore A23187 was assessed. Results Fentanyl (0.297 x 10 0.785 x 10 m) attenuated acetylcholine-induced vasorelaxation in ring preparations with or without 10 m naloxone. Pirenzepine (10 to 10 m) and 4-diphenylacetoxyl-N-methylpiperidine methiodide (10 to 10 m) produced a parallel rightward shift in the acetylcholine concentration-response curve. The concentrations (-log M) of pirenzepine and 4-diphenylacetoxyl-N-methylpiperidine methiodide necessary to displace the concentration-response curve of an acetylcholine by twofold were estimated to be 6.886 +/- 0.070 and 9.256 +/- 0.087, respectively. Methoctramine, 10 m, did not alter the acetylcholine concentration-response curve. Fentanyl, 0.785 x 10 m, attenuated acetylcholine-induced vasorelaxation in the rings pretreated with 10 m pirenzepine but had no effect on vasorelaxation in the rings pretreated with 10 m 4-diphenylacetoxyl-N-methylpiperidine methiodide. Fentanyl, 0.785 x 10 m, did not significantly alter calcium ionophore A23187-induced vasorelaxation. Conclusions These results indicate that fentanyl attenuates acetylcholine-induced vasorelaxation via an inhibitory effect at a level proximal to nitric oxide synthase activation on the pathway involving endothelial M3 muscarinic receptor activation in rat aorta.

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