Differences between negative inotropic and vasodilator effects of calcium antagonists acting on extra- and intracellular calcium movements in rat and guinea-pig cardiac preparations

1989 ◽  
Vol 340 (5) ◽  
pp. 567-575 ◽  
Author(s):  
J. G. Hugtenburg ◽  
M.-J. Mathy ◽  
H. W. G. M. Boddeke ◽  
J. J. Beckeringh ◽  
P. A. van Zwieten
1985 ◽  
Vol 63 (1) ◽  
pp. 23-29 ◽  
Author(s):  
Melissa A. Damiano ◽  
Edward J. Barbieri

The effects of three calcium antagonists, verapamil, lanthanum, and 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate (TMB-8) were studied on the release of slow-reacting substance of anaphylaxis (SRS-A) from ovalbumin-sensitized chopped guinea pig lung parenchyma in calcium-containing and calcium-free media. The SRS-A levels (mean ± SEM) obtained from tissues incubated in normal and calcium-free Krebs–bicarbonate buffer were 51 ± 8 (N = 19) and 21 ± 4 (N = 14) U/mL, respectively. TMB-8 (0.1–10 μM) a reported intracellular calcium antagonist, reduced antigen-stimulated SRS-A release from lung tissue incubated in calcium-containing, but not calcium-free, medium; A23187-induced SRS-A release from normal guinea pig lung was not significantly altered by TMB-8 at concentrations up to 10 μM. Verapamil and lanthanum consistently reduced SRS-A release only at high concentrations (100 μM and 1 mM, respectively). The quantities of SRS-A released from lung tissue incubated in the presence of verapamil in normal medium were similar to those obtained in calcium-free medium. Tissues incubated in the presence of potassium chloride (60 and 100 mM) did not release significant quantities of SRS-A, and release which did occur was not blocked by verapamil, suggesting that antigen-induced SRS-A release is not dependent on membrane depolarization and that verapamil was not exerting inhibition via blockade of voltage-dependent calcium channels. These data suggest that although intracellular calcium is important for the regulation of SRS-A secretion from guinea pig lung tissue, extracellular calcium is necessary for optimal release of SRS-A.


Life Sciences ◽  
1980 ◽  
Vol 27 (24) ◽  
pp. 2339-2346 ◽  
Author(s):  
Stanley R. Jolly ◽  
Lawrence A. Menahan ◽  
Garrett J. Gross

ORL ◽  
1991 ◽  
Vol 53 (2) ◽  
pp. 78-81 ◽  
Author(s):  
Katsuhisa Ikeda ◽  
Yoshitaka Saito ◽  
Akinori Nishiyama ◽  
Tomonori Takasaka

1993 ◽  
Vol 45 (2) ◽  
pp. 407-414 ◽  
Author(s):  
Philip A. Iredale ◽  
Keith F. Martin ◽  
Stephen J. Hill ◽  
David A. Kendall

2014 ◽  
Vol 58 (2) ◽  
pp. 199-210 ◽  
Author(s):  
Elżbieta Bednarska

It is shown that callose synthesis in the <em>Oenothera biennis </em>pollen tube is regulated by the endogenous Ca<sup>2+</sup> level. Calcium antagonists reduced the amount of callose in the wall above the tip of the pollen tube (Verapamil - calcium channels blocker) and at the tube tip after stopping tube growth (La<sup>3+</sup> - a Ca<sup>2+</sup> substitute). Ruthenium red and ionophore A 23187, which raise the Ca 21 level in the cytoplasm, induced callose synthesis at the tip of pollen tube.


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