کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5827932 | 1558943 | 2014 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
L-type Ca2+ channel blockers inhibit the window contraction of mouse aorta segments with high affinity
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کلمات کلیدی
VSMIC50DepolarizationNifedipine (PubChem CID: 4485)L-NNALCCSl-NAME - L-NAMENω-nitro-l-arginine - N-NITRO-L-ARGININENω-nitro-l-arginine methyl ester - N-Nitro-L-Arginine Methyl EsterContraction - اختصارVascular smooth muscle - عضله صاف عضلانیCalcium channel blocker - مسدود کننده کانال کلسیمNitric oxide - نیتریک اکسیدVascular reactivity - واکنش پذیری عروقیL-type calcium channels - کانال های کلسیم L نوعL-type calcium channel - کانال کلسیم L نوع
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب سلولی و مولکولی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: L-type Ca2+ channel blockers inhibit the window contraction of mouse aorta segments with high affinity L-type Ca2+ channel blockers inhibit the window contraction of mouse aorta segments with high affinity](/preview/png/5827932.png)
چکیده انگلیسی
L-type calcium channel blockers (LCCBs) reduce blood pressure more effectively in hypertensive than in normotensive subjects and are more effective in vascular smooth muscle (VSM) than in cardiac muscle. This has been explained by the depolarized resting potential of VSM in comparison with heart muscle cells and during hypertension, because both favor the “high affinity” inactivated state of the L-type calcium channel (LCC). Depolarized resting potentials, however, also increase Ca2+ influx via window, non-inactivating LCC. The present study investigated whether these channels can be effectively blocked by nifedipine, verapamil or diltiazem, as representatives of different LCCB classes. C57Bl6 mouse aortic segments were depolarized by 50Â mM K+ to attain similar degree of inactivation. The depolarization evoked biphasic contractions with the slow force component displaying higher sensitivity to LCCBs than the fast component. Removal of the fast force component increased, whereas stimulation of Ca2+ influx with the dihydropyridine BAY K8644, a structural analog of nifedipine, decreased the efficacy of the LCCBs. Addition of LCCBs during the contraction caused concentration-dependent relaxation, which was independent of the presence of a fast force component, but still showed lower sensitivity in the presence of BAY K8644. Our data suggest that steady-state contractions by depolarization with 50Â mM K+ are completely due to window Ca2+ influx, which is preferentially inhibited by LCCBs. Furthermore, results point to interactions between the LCCB receptors and Ca2+ ions or BAY K8644. The high affinity for open, non-inactivating LCC may play a dominant role in the anti-hypertensive effects of LCCBs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: European Journal of Pharmacology - Volume 738, 5 September 2014, Pages 170-178
Journal: European Journal of Pharmacology - Volume 738, 5 September 2014, Pages 170-178
نویسندگان
Cédéric F. Michiels, Cor E. Van Hove, Wim Martinet, Guido R.Y. De Meyer, Paul Fransen,