Stereoselectivity of butylidenephthalide on non-adrenergic prejunctional voltage-dependent Ca 2+ channels in prostatic portion of rat vas deferens

2016 ◽  
Vol 786 ◽  
pp. 47-52 ◽  
Author(s):  
Chung-Hung Shih ◽  
Chi-Ming Chen ◽  
Wun-Chang Ko
1996 ◽  
Vol 270 (5) ◽  
pp. C1468-C1477 ◽  
Author(s):  
M. A. Khoyi ◽  
T. Ishikawa ◽  
K. D. Keef ◽  
D. P. Westfall

The present study investigates how changes in intracellular Ca2+ concentration modulate the influx of 45Ca2+ in isolated rat vasa deferentia. Raising extracellular K+ concentration ([K+]0) to > or = 32 mM increased 45Ca2+ influx during the 1st min in solutions containing 0.03-1.5 mM extracellular Ca2+ concentration ([Ca2+]0). During the 6th min in [K+]0 > or = 50 mM, 45Ca2+ influx was less than during the 1st min. This decline in 45Ca2+ influx occurred for [Ca2+]0 > or = 0.4 mM. Procaine potentiated K(+)-stimulated 45Ca2+ influx in 1.5 mM [Ca2+]0 and eliminated the decline of 45Ca2+ influx in low [Ca2-]0. Ryanodine and norepinephrine reduced K(+)-stimulated 45Ca2+ influx. 45Ca2+ content changed with time in accordance with the changes observed in 45Ca2+ influx. In isolated cells, voltage-dependent inward currents inactivated more rapidly with 1.5 mM Ca2+ as the charge carrier than with 1.5 mM Ba2+, and the steady-state inactivation relationship was shifted in the hyperpolarizing direction. Inward current was reduced with either caffeine, ryanodine, or norepinephrine. The inhibitory effects of norepinephrine were abolished by depletion of intracellular Ca2+ stores. These results are compatible with the hypothesis that K(+)-stimulated 45Ca2+ influx declines with time due to Ca(2+)-induced inhibition of Ca2- channels. Ca(2+)- and inositol 1,4,5-trisphosphate-induced releases of Ca2+ from the sarcoplasmic reticulum appear to play an important role in this process.


1991 ◽  
Vol 41 (8) ◽  
pp. 1107-1110 ◽  
Author(s):  
JoséM. Lizcano ◽  
Dolors Balsa ◽  
Keith F. Tipton ◽  
Mercedes Unzeta

Nature ◽  
1970 ◽  
Vol 228 (5271) ◽  
pp. 564-565 ◽  
Author(s):  
K. NISHINO ◽  
T. IRIKURA ◽  
I. TAKAYANAGI

1997 ◽  
Vol 325 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Yu Huang ◽  
C.-W. Lau ◽  
I.H.M. Ho

1998 ◽  
Vol 192 (4) ◽  
pp. 489-495 ◽  
Author(s):  
G. D. PAPWORTH ◽  
P. M. DELANEY ◽  
L. J. BUSSAU ◽  
L. T. VO ◽  
R. G. KING

2014 ◽  
Vol 387 (8) ◽  
pp. 719-731 ◽  
Author(s):  
Edilson Dantas da Silva Júnior ◽  
Juliano Quintella Dantas Rodrigues ◽  
Bruno Palmieri de Souza ◽  
Afonso Caricati-Neto ◽  
Aron Jurkiewicz ◽  
...  

1976 ◽  
Vol 54 (3) ◽  
pp. 412-416 ◽  
Author(s):  
D. M. Paton ◽  
J. Buckland-Nicks ◽  
A. Johns

Tissues from the duodenum and vas deferens of Sprague–Dawley rats were examined of the rat vas deferens and gap junctions. Can. J. Physiol. Pharmacol. 54, 412–416. by electron microscopy after glutaraldehyde fixation and postosmication. Gap junctions (nexuses) were readily demonstrated in the duodenum in both control and reserpine treated animals (1.0 mg/kg per day for 7 days). However, gap junctions could not be demonstrated in vas deferens. It is concluded that the postjunctional supersensitivity and spontaneous activity induced by reserpine in vas deferens, does not result from the formation of gap junctions.


1967 ◽  
Vol 19 (10) ◽  
pp. 695-695 ◽  
Author(s):  
Stella R. O'Donnell ◽  
Sally E. Hecker

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