scholarly journals Effects Of F-18 On KCL And Phenylephrine - Induced Contractions Of Rat Aorta

Author(s):  
Abdisalim Zaripov ◽  
◽  
Adilbay Esimbetov ◽  
Pulat Usmanov ◽  
Durdona Shokirova ◽  
...  

The mechanism of action of the alkaloid 1-(2´-bromine-4´,5´-dimethoxyphenyl) - 6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline (F-18) on the functional activity of smooth muscle cells of the rat aorta was studied. Isometric contraction activity was recorded using a Grass FT – 03 (Grass Instrument, USA) mechanotron. The relaxant effect of the F-18 alkaloid was found to be associated with blockade of Ca2 + (IP3R) channels in the SR, along with voltage- dependent and receptor-operated Ca2+channels in the aorta smooth muscle cell plasmalemma.

1995 ◽  
Vol 268 (2) ◽  
pp. H544-H549 ◽  
Author(s):  
Y. Hirakawa ◽  
T. Kuga ◽  
S. Kobayashi ◽  
H. Kanaide ◽  
A. Takeshita

The purpose of the present study was to investigate regulation of voltage-dependent Ca2+ channels by serotonin in rat aortic smooth muscle cells in primary culture. L- and T-type Ca2+ currents (ICa) were recorded using the whole cell voltage-clamp method. Without pretreatment, in 25 of 30 cells examined, 10 microM serotonin decreased L-type ICa to various extents (-14 to -72%). However, in the remaining five cells, serotonin increased L-type ICa 21 +/- 4%. Thus, in 30 cells, serotonin decreased L-type ICa an average of 22 +/- 5%. In the presence of intracellular heparin (100 micrograms/ml), a blocker of inositol 1,4,5-trisphosphate binding to its receptor, serotonin increased L-type ICa in all cells 29 +/- 3% (n = 6). When stored Ca2+ was depleted by pretreatment either with 20 microM ryanodine and 20 mM caffeine or with 100 nM A-23187, serotonin also increased L-type ICa in all cells 30 +/- 5 (n = 4) or 37 +/- 5% (n = 12), respectively. In the presence of heparin, the serotonin-induced increase of L-type ICa was prevented by 100 nM staurosporine (2 +/- 3%; n = 6, P < 0.01). The serotonin-induced decrease of L-type ICa was significantly augmented by 100 nM staurosporine (-43 +/- 10%; n = 5). Phorbol 12,13-dibutylate (PDBu; 1 microM) increased L-type ICa 29 +/- 3% (n = 6), and serotonin did not further increase L-type ICa after its potentiation by PDBu.(ABSTRACT TRUNCATED AT 250 WORDS)


1999 ◽  
Vol 79 ◽  
pp. 274
Author(s):  
Kenji Shirotani ◽  
Atsuo Hara ◽  
Atsuko Higo ◽  
Chihaya Tammi ◽  
Masashi Katsura ◽  
...  

1989 ◽  
Vol 92 (1) ◽  
pp. 61-63
Author(s):  
sadoshima Jun-Ichi ◽  
Akaike Norio ◽  
Tomoike Hitonobu ◽  
Kanaide Hideo ◽  
Nakamura Motoomi

1990 ◽  
Vol 67 (2) ◽  
pp. 469-480 ◽  
Author(s):  
T Kuga ◽  
J Sadoshima ◽  
H Tomoike ◽  
H Kanaide ◽  
N Akaike ◽  
...  

1994 ◽  
Vol 266 (4) ◽  
pp. C975-C980 ◽  
Author(s):  
F. Zhang ◽  
J. L. Ram ◽  
P. R. Standley ◽  
J. R. Sowers

Previous studies have shown that 17 beta-estradiol (beta-E2) has a direct acute inhibitory effect on vascular smooth muscle (VSM) contraction. To investigate the mechanisms underlying this phenomenon, we utilized whole cell patch-clamping techniques to study effects of beta-E2 on voltage-dependent Ca2+ channels in cultured VSM cells (VSMC). T- and L-type Ca2+ currents were characterized with ramp and pulse protocols in A7r5 cultured VSMC. T-type current, inactivated in < 100 ms, was reduced by Ba2+ and was comparatively little affected by isradipine. L-type current required higher voltages to activate, inactivated slowly, was greatly increased by Ba2+, and could be completely inhibited by 5 microM isradipine. beta-E2 (10 microM) significantly reduced peak L-type Ba2+ current and T-type Ca2+ current within 1-2 min, whereas alpha E2 (a hormonally inactive isomer of estradiol) caused significantly less reduction in both types of current. Vehicle (0.1% ethanol) had no significant effect on either current. The inhibitory effect of beta-E2 on voltage-dependent Ca2+ currents may contribute to previously demonstrated beta-E2 attenuation of VSM contraction.


Sign in / Sign up

Export Citation Format

Share Document