Alteration of the Calcium Content in Inner Hair Cells of the Cochlea of the Guinea Pig after Acute Noise Trauma with and without Application of the Organic Calcium Channel Blocker Diltiazem

ORL ◽  
1999 ◽  
Vol 61 (6) ◽  
pp. 328-333 ◽  
Author(s):  
Jan Maurer ◽  
Ulf-Rüdiger Heinrich ◽  
MichaelL. Hinni ◽  
Wolf Mann
Keyword(s):  
Guinea Pig ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Hair Cells ◽  
Channel Blocker ◽  
Calcium Content ◽  
Noise Trauma ◽  
Inner Hair Cells

Radiosynthesis of dimethyl-2-[18F]-(fluoromethyl)-6-methyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate for L-type calcium channel imaging

2008 ◽  
Vol 96 (12) ◽  
Author(s):  
H. Sadeghpour ◽  
A. R. Jalilian ◽  
A. Shafiee ◽  
M. Akhlaghi ◽  
R. Miri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Muscle Model ◽  
Channel Distribution ◽  
Longitudinal Smooth Muscle ◽  
Biological Studies

AbstractDimethyl 2-(fluoromethyl)-6-methyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate 4a, a fluorinated nifedipine analog, has been shown to elicit significant calcium channel blocker activity using a guinea pig ileal longitudinal smooth muscle model. In order to perform biological studies for detection of L-type calcium channel distribution, we decided to prepare the [

Interaction of a calcium channel blocker with noise in cochlear function in guinea pig

2012 ◽  
Vol 132 (11) ◽  
pp. 1140-1144 ◽  
Author(s):  
Jun Liu ◽  
Yu-Guang Niu ◽  
Wan- Xin Li ◽  
Yong-Yi Yuan ◽  
Wei-Ju Han ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Cochlear Function

Verapamil corrects abnormalities in norepinephrine metabolism of brain synaptosomes in CRF

1990 ◽  
Vol 258 (4) ◽  
pp. F1036-F1041
Author(s):  
M. Smogorzewski ◽  
A. Islam ◽  
R. Minasian ◽  
A. R. Soliman ◽  
S. G. Massry
Keyword(s):  
Renal Failure ◽  
Parathyroid Hormone ◽  
Atpase Activity ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Calcium Content ◽  
Norepinephrine Metabolism ◽  
Brain Synaptosomes ◽  
Effect Of Treatment

Abnormalities in norepinephrine (NE) metabolism of brain synaptosomes occur in chronic renal failure (CRF), and this has been attributed to the parathyroid hormone (PTH)-induced accumulation of calcium in synaptosomes. The present study examined the effect of treatment with the calcium-channel blocker verapamil on NE content, release, and uptake, on Na(+)-K(+)-ATPase activity, and on calcium content of brain synaptosomes from rats with 21 days of CRF. Verapamil treatment of normal rats for 21 days did not affect synaptosomal NE content, release, or uptake, Na(+)-K(+)-ATPase activity, or calcium content. Rats with 21 days of CRF displayed a significant (P less than 0.01) reduction in their synaptosomal NE content, release, and uptake, an increase in Na(+)-K(+)-ATPase activity, and a significant (P less than 0.01) increase in calcium content of synaptosomes. The treatment of CRF rats with verapamil normalized synaptosomal NE content and release and Na(+)-K(+)-ATPase activity, produced a significant (P less than 0.01) improvement in NE uptake, and prevented the accumulation of calcium in synaptosomes. The data of the present study are consistent with the notion that the abnormalities in synaptosomal NE metabolism and Na(+)-K(+)-ATPase in CRF are mainly the result of PTH-induced accumulation of calcium in synaptosomes and could be prevented by a calcium-channel blocker.

Chronic treatment by the calcium channel blocker ± PN 200-110 in the rat counteracts the stimulations of pituitary weight, prolactin release and pituitary C-kinase activity induced by a chronic estradiol treatment, in vivo

1990 ◽  
Vol 122 (3) ◽  
pp. 403-408
Author(s):  
Ph. Touraine ◽  
P. Birman ◽  
F. Bai-Grenier ◽  
C. Dubray ◽  
F. Peillon ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Protein Kinase ◽  
Calcium Channel ◽  
Calcium Channel Blocker ◽  
Channel Blocker ◽  
Plasma Prolactin ◽  
Estradiol Treatment ◽  
Kinase C ◽  
Protein Kinase C Activity

Abstract In order to investigate whether a calcium channel blocker could modulate the protein kinase C activity in normal and estradiol pretreated rat pituitary, female Wistar rats were treated or not (controls) with ± PN 200-110 (3 mg · kg−1 · day−1, sc) for 8 days or with estradiol cervical implants for 8 or 15 days, alone or in combination with PN 200-110 the last 8 days. Estradiol treatment induced a significant increase in plasma prolactin levels and pituitary weight. PN 200-110 administered to normal rats did not modify these parameters, whereas it reduced the effects of the 15 days estradiol treatment on prolactin levels (53.1 ± 4.9 vs 95.0 ±9.1 μg/l, p<0.0001) and pituitary weight (19.9 ± 0.4 vs 23.0 ± 0.6 mg, p <0.001), to values statistically comparable to those measured after 8 days of estradiol treatment. PN 200-110 alone did not induce any change in protein kinase C activity as compared with controls. In contrast, PN 200-110 treatment significantly counteracted the large increase in soluble activity and the decrease in the particulate one induced by estradiol between day 8 and day 15. We conclude that PN 200-110 opposed the stimulatory effects of chronic in vivo estradiol treatment on plasma prolactin levels and pituitary weight and that this regulation was related to a concomitant modulation of the protein kinase C activity.

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