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Depolarization-induced calcium influx in rat mesenteric small arterioles is mediated exclusivelyviamibefradil-sensitive calcium channels
| Content Provider | Scilit |
|---|---|
| Author | Jensen, Lars J. Salomonsson, Max Jensen, Boye L. Holstein-Rathlou, Niels-Henrik |
| Copyright Year | 2004 |
| Description | Journal: British Journal of Pharmacology |
| Abstract | In this study, intracellular $Ca^{2+}$ was measured as the Fura‐2 ratio (R) of fluorescence excited at 340 and 380 nm $(F_{340}/F_{380}$) in nonpressurized rat mesenteric small arterioles (Ø (lumen diameter) 10–25 μm). The response to depolarization using 75 mM KCl was an increase in R from a baseline of 0.96±0.01 ([Ca^{2+}$]_{i}$ ∼74 nM) to 1.04±0.01 (∼128 nM) (n=80). The response to 75 mM $K^{+}$ was reversibly abolished in $Ca^{2+}$‐free physiological saline solution, whereas phentolamine (10 μM) or tetrodotoxin (1 μM) had no effects. $LaCl_{3}$ (200 μM) inhibited 61±9% of the response. A $[K^{+}$]‐response curve indicated that the $Ca^{2+}$ response was activated between 15 and 25 mM $K^{+}$. The data suggest that the $Ca^{2+}$ response was caused by the activation of voltage‐dependent $Ca^{2+}$ channels. Mibefradil use dependently inhibited the $Ca^{2+}$ response to 75 mM $K^{+}$ by 29±2% (100 nM), 73±7% (1 μM) or 89±7% (10 μM). Pimozide (500 nM) use dependently inhibited the $Ca^{2+}$ response by 85±1%. Nifedipine (1 μM) inhibited the $Ca^{2+}$ response to 75 mM $K^{+}$ by 41±12%. The response was not inhibited by calciseptine (500 nM), ω‐agatoxin IVA (100 nM), ω‐conotoxin MVIIA (500 nM), or SNX‐482 (100 nM). Using reverse transcriptase–polymerase chain reaction, it was shown that neither $Ca_{V}$2.1a (P‐type) nor $Ca_{V}$2.1b (Q‐type) voltage‐dependent $Ca^{2+}$ channels were expressed in mesenteric arterioles, whereas the $Ca_{V}$3.1 (T‐type) channel was expressed. Furthermore, no amplification products were detected when using specific primers for the $β_{1b}$, $β_{2}$, or $β_{3}$ auxiliary subunits of high‐voltage‐activated $Ca^{2+}$ channels. The results suggest that the voltage‐dependent $Ca^{2+}$ channel activated by sustained depolarization in mesenteric arterioles does not classify as any of the high‐voltage‐activated channels (L‐, P/Q‐, N‐, or R‐type), but is likely to be a T‐type channel. The possibility that the sustained $Ca^{2+}$ influx observed was the result of a T‐type window current is discussed. British Journal of Pharmacology (2004) 142, 709–718. doi:10.1038/sj.bjp.0705841 |
| Related Links | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1575051/pdf |
| Ending Page | 718 |
| Page Count | 10 |
| Starting Page | 709 |
| e-ISSN | 14765381 |
| DOI | 10.1038/sj.bjp.0705841 |
| Journal | British Journal of Pharmacology |
| Issue Number | 4 |
| Volume Number | 142 |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 2004-06-01 |
| Access Restriction | Open |
| Subject Keyword | Journal: British Journal of Pharmacology Resistance Vessel Vascular Smooth Muscle Cell Voltage-dependent Ca2+ Channel Conducted Vascular Response |
| Content Type | Text |
| Resource Type | Article |
