Comparative Effects of Chronic Exposure to Ethanol and Calcium Channel Antagonists on Calcium Channel Antagonist Receptors in Cultured Neural (PC12) Cells

1989 ◽  
Vol 53 (1) ◽  
pp. 168-172 ◽  
Author(s):  
Shelley S. Marks ◽  
Daniel L. Watson ◽  
Celia L. Carpenter ◽  
Robert O. Messing ◽  
David A. Greenberg
2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Shiwan K. Shah ◽  
Sanjeev Kumar Goswami ◽  
Rajesh V. Babu ◽  
Gulshan Sharma ◽  
Alexander G. Duarte

Calcium channel antagonists (CCAs) are commonly involved in drug overdoses. Standard approaches to the management of CCA overdoses, including fluid resuscitation, gut decontamination, administration of calcium, glucagon, and atropine, as well as supportive care, are often ineffective. We report on two patients who improved after addition of hyperinsulinemia-euglycemia (HIE) therapy. We conclude with a literature review on hyperinsulinemia-euglycemia therapy with an exploration of the physiology behind its potential use.


1992 ◽  
Vol 118 (3) ◽  
pp. 663-670 ◽  
Author(s):  
J L Saffell ◽  
F S Walsh ◽  
P Doherty

We present evidence that direct activation of neuronal second messenger pathways in PC12 cells by opening voltage-dependent calcium channels mimics cell adhesion molecule (CAM)-induced differentiation of these cells. PC12 cells were cultured on monolayers of control 3T3 cells or 3T3 cells expressing transfected N-cadherin in the presence of KCl or a calcium channel agonist Bay K 8644. Both potassium depolarization and agonist-induced activation of calcium channels promoted substantial neurite outgrowth from PC12 cells cultured on control 3T3 monolayers and increased neurite outgrowth from those cultured on N-cadherin-expressing 3T3 monolayers. The potassium-induced response could be inhibited by L- and N-type calcium channel antagonists and by kinase inhibitor K-252b but was unaffected by pertussis toxin. In contrast activators of protein kinase C did not stimulate neurite outgrowth, and the neurite outgrowth response induced by activation of protein kinase A was not inhibited by calcium channel antagonists or pertussis toxin. These studies support the postulate that CAM-induced neuronal differentiation involves a specific transmembrane signaling pathway and suggest that activation of this pathway after CAM binding may be more important for the neurite outgrowth response than CAM-dependent adhesion per se.


Hypertension ◽  
1995 ◽  
Vol 26 (1) ◽  
pp. 143-149 ◽  
Author(s):  
Mala T. Kailasam ◽  
Robert J. Parmer ◽  
Justine H. Cervenka ◽  
Regina A. Wu ◽  
Michael G. Ziegler ◽  
...  

Author(s):  
M. Bidya Sagar ◽  
K. Ravikumar ◽  
Y. S. Sadanandam

AbstractThe crystallographic characterization of the following three calcium channel antagonists is reported here: 2,6-dimethyl-3,5-dicarbamoyl-4-[2-nitro]-1,4-dihydropyridine (


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