JPET Celsis microsomes equal better data

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Furukawa, T.
Right arrow Articles by Nukada, T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Furukawa, T.
Right arrow Articles by Nukada, T.

Vol. 291, Issue 2, 464-473, November 1999

Selectivities of Dihydropyridine Derivatives in Blocking Ca2+ Channel Subtypes Expressed in Xenopus Oocytes1

Taiji Furukawa, Takeshi Yamakawa, Takayuki Midera, Toshio Sagawa, Yasuo Mori and Toshihide Nukada

Department of Medicine, Teikyo University School of Medicine, Tokyo, Japan (T.F., T.Y., T.M., T.S.); Department of Information Physiology, National Institute for Physiological Sciences, Okazaki, Japan (Y.M.); and Department of Neurochemistry, Tokyo Institute of Psychiatry, Tokyo, Japan (T.N.)

Some dihydropyridines (DHPs), such as amlodipine and cilnidipine, have been shown to block not only L-type but also N-type Ca2+ channels; therefore, DHPs are no longer considered as L-type-specific Ca2+ channel blockers. However, selectivity of DHPs for Ca2+ channel subtypes including N-, P/Q-, and R-types are poorly understood. To address this issue at the molecular level, blocking effects of 10 DHPs (nifedipine, nilvadipine, barnidipine, nimodipine, nitrendipine, amlodipine, nicardipine, benidipine, felodipine, and cilnidipine) on four subtypes of Ca2+ channels (L-, N-, P/Q-, and R-types) were investigated in the Xenopus oocyte expression system with the use of the two-microelectrode voltage-clamp technique. L-type Ca2+ channels expressed as alpha 1Calpha 2beta 1a combination were profoundly blocked by all DHPs examined, whereas blocking actions of these DHPs on R-type (alpha 1Ealpha 2beta 1a) channels were equally weak. In contrast, 5 of the 10 DHPs (amlodipine, benidipine, cilnidipine, nicardipine, and barnidipine) significantly blocked N-type (alpha 1Balpha 2beta 1a) and P/Q-type (alpha 1Aalpha 2beta 1a) Ca2+ channels. These selectivities of DHPs in blocking Ca2+ channel subtypes would provide useful pharmacological and clinical information on the mode of action of the drugs including side effects and adverse effects.

0022-3565/99/2912-0464$03.00/0
THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS
Copyright © 1999 by The American Society for Pharmacology and Experimental Therapeutics


This article has been cited by other articles:


Home page
 Circ. Res.Home page
K. Hayashi, S. Wakino, N. Sugano, Y. Ozawa, K. Homma, and T. Saruta
Ca2+ Channel Subtypes and Pharmacology in the Kidney
Circ. Res., February 16, 2007; 100(3): 342 - 353.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
D. Andreasen, U. G. Friis, T. R. Uhrenholt, B. L. Jensen, O. Skott, and P. B. Hansen
Coexpression of Voltage-Dependent Calcium Channels Cav1.2, 2.1a, and 2.1b in Vascular Myocytes
Hypertension, April 1, 2006; 47(4): 735 - 741.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
J. A. Goldberg and C. J. Wilson
Control of Spontaneous Firing Patterns by the Selective Coupling of Calcium Currents to Calcium-Activated Potassium Currents in Striatal Cholinergic Interneurons
J. Neurosci., November 2, 2005; 25(44): 10230 - 10238.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
D. J. Adams, A. B. Smith, C. I. Schroeder, T. Yasuda, and R. J. Lewis
omega -Conotoxin CVID Inhibits a Pharmacologically Distinct Voltage-sensitive Calcium Channel Associated with Transmitter Release from Preganglionic Nerve Terminals
J. Biol. Chem., January 31, 2003; 278(6): 4057 - 4062.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
M. Day, P. A. Olson, J. Platzer, J. Striessnig, and D. J. Surmeier
Stimulation of 5-HT2 Receptors in Prefrontal Pyramidal Neurons Inhibits Cav1.2 L-Type Ca2+ Currents Via a PLCbeta /IP3/Calcineurin Signaling Cascade
J Neurophysiol, May 1, 2002; 87(5): 2490 - 2504.
[Abstract] [Full Text] [PDF]

Home page
 Antimicrob. Agents Chemother.Home page
U. Wenzel, S. Kuntz, S. Diestel, and H. Daniel
PEPT1-Mediated Cefixime Uptake into Human Intestinal Epithelial Cells Is Increased by Ca2+ Channel Blockers
Antimicrob. Agents Chemother., May 1, 2002; 46(5): 1375 - 1380.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Renal Physiol.Home page
T. Yamamoto, Y. Tomura, H. Tanaka, and F. Kajiya
In vivo visualization of characteristics of renal microcirculation in hypertensive and diabetic rats
Am J Physiol Renal Physiol, September 1, 2001; 281(3): F571 - F577.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurophysiol.Home page
D. C. Bell, A. J. Butcher, N. S. Berrow, K. M. Page, P. F. Brust, A. Nesterova, K. A. Stauderman, G. R. Seabrook, B. Nurnberg, and A. C. Dolphin
Biophysical Properties, Pharmacology, and Modulation of Human, Neuronal L-Type ({alpha}1D, CaV1.3) Voltage-Dependent Calcium Currents
J Neurophysiol, February 1, 2001; 85(2): 816 - 827.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
K. A. Fagan, R. A. Graf, S. Tolman, J. Schaack, and D. M. F. Cooper
Regulation of a Ca2+-sensitive Adenylyl Cyclase in an Excitable Cell. ROLE OF VOLTAGE-GATED VERSUS CAPACITATIVE Ca2+ ENTRY
J. Biol. Chem., December 15, 2000; 275(51): 40187 - 40194.
[Abstract] [Full Text] [PDF]


Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
Molecular Interventions Drug Metabolism and Disposition

Copyright © 1999 by the American Society for Pharmacology and Experimental Therapeutics.