Comparative action of flunarizine, phenytoin, carbamazepine and two calcium-entry blockers on spontaneous epileptiforrn bursts in the low calcium-hippocampal slice preparation

1986 ◽  
Vol 8 (1-4) ◽  
pp. 397-405 ◽  
Author(s):  
David Ashton ◽  
Kenneth Reid ◽  
Roland Willems ◽  
Roger Marrannes ◽  
Albert Wauquier
Keyword(s):  
Hippocampal Slice ◽  
Calcium Entry ◽  
Calcium Entry Blockers ◽  
Slice Preparation ◽  
Low Calcium ◽  
Comparative Action

KCl and angiotensin responses in isolated rat renal arterioles: effects of diltiazem and low-calcium medium

1993 ◽  
Vol 264 (1) ◽  
pp. F134-F140 ◽  
Author(s):  
J. D. Conger ◽  
S. A. Falk
Keyword(s):  
Cytosolic Calcium ◽  
Calcium Entry ◽  
Ang Ii ◽  
Calcium Entry Blockers ◽  
Bathing Medium ◽  
Primary Mechanism ◽  
Low Calcium ◽  
Intracellular Calcium Mobilization ◽  
Constrictor Response ◽  
Isolated Rat

Studies in intact renovascular models have shown that calcium entry blockers inhibit angiotensin (ANG II)-induced vasoconstriction in afferent (AA) but not efferent arterioles (EA), suggesting that increases in smooth muscle cell cytosolic calcium, the initiating intracellular message, result from entry through potential-operated channels in AA, but from organelle storage mobilization or entry through nonpotential-operated channels in EA. The present study examined the effects of diltiazem (10(-5) M) on the constrictor responses to KCl (50 mM) and half-maximal constricting concentrations (EC50) of ANG II and the effects of low-calcium bathing medium on EC50 ANG II responses in isolated rat AA and EA. KCl caused slightly greater decreases in lumen diameter in AA than in EA (P < 0.05) that were completely inhibited by diltiazem in both. Vasoconstriction to ANG II was significantly inhibited by diltiazem (29 +/- 12 vs. 67 +/- 31%; P < 0.02) in AA. However, constrictor response to ANG II in EA was unchanged by diltiazem (42 +/- 32 vs. 41 +/- 31%). Constriction to ANG II of AA in low-calcium medium was significantly attenuated (8 +/- 13 vs. 54 +/- 12%; P < 0.01); however, EA constrictor response was not affected (43 +/- 22 vs. 51 +/- 19%). These data indicate that EC50 ANG II-induced AA constriction requires calcium entry primarily through potential-operated channels. While potential-operated calcium entry channels can be functionally expressed in EA, intracellular calcium mobilization is the primary mechanism for ANG II-induced constriction.

scholarly journals A new class of calcium entry blockers defined by 1,3-diphosphonates

1989 ◽  
Vol 264 (28) ◽  
pp. 16598-16607
Author(s):  
J R Rossier ◽  
J A Cox ◽  
E J Niesor ◽  
C L Bentzen
Keyword(s):  
Calcium Entry ◽  
Calcium Entry Blockers ◽  
New Class

Different effects of R 56865 and calcium entry blockers on K+- and noradrenaline-induced contractions and 45Ca uptake in rat aorta

1988 ◽  
Vol 158 (3) ◽  
pp. 183-190 ◽  
Author(s):  
Peter Koch ◽  
Doris Wilhelm ◽  
Detlef Wermelskirchen ◽  
Ute Nebel ◽  
Bob Wilffert ◽  
...  
Keyword(s):  
Rat Aorta ◽  
Calcium Entry ◽  
Calcium Entry Blockers ◽  
45Ca Uptake ◽  
R 56865

Folic acid has a disinhibitory action in the rat hippocampal slice preparation

1985 ◽  
Vol 346 (2) ◽  
pp. 281-286 ◽  
Author(s):  
Laura C. Otis ◽  
Daniel V. Madison ◽  
Roger A. Nicoll
Keyword(s):  
Folic Acid ◽  
Hippocampal Slice ◽  
Slice Preparation

Possible Role of Calcium Entry Blockers in Brain Protection

1986 ◽  
Vol 25 (1) ◽  
pp. 102-114 ◽  
Author(s):  
A. Baethmann ◽  
M. Jansen
Keyword(s):  
Calcium Entry ◽  
Brain Protection ◽  
Calcium Entry Blockers

The Hippocampal Slice Preparation

2019 ◽  
pp. 211-226
Author(s):  
Larry G. Stark ◽  
Timothy E. Albertson
Keyword(s):  
Hippocampal Slice ◽  
Slice Preparation
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