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Thapsigargin- and cyclopiazonic acid-induced endothelium-dependent hyperpolarization in rat mesenteric artery
| Content Provider | Scilit |
|---|---|
| Author | Fukao, Mitsuhiro Hattori, Yuichi Kanno, Morio Sakuma, Ichiro Kitabatake, Akira |
| Copyright Year | 1995 |
| Description | Journal: British Journal of Pharmacology 1 The present study was designed to determine whether putative, selective inhibitors of the $Ca^{2+}$–pump ATPase of endoplasmic reticulum, thapsigargin (TSG) and cyclopiazonic acid (CPA), induce endothelium-dependent hyperpolarization in the rat isolated mesenteric artery. The membrane potentials of smooth muscle cells of main superior mesenteric arteries were measured by the microelectrode technique. 2 In tissues with endothelium, TSG $(10^{−8}–10^{−5}$m) caused sustained hyperpolarization in a concentration-dependent manner. In tissues without endothelium, TSG did not cause any change in membrane potential. CPA $(10^{−5}$ m) also hyperpolarized the smooth muscle membrane, an effect that was endothelium-dependent and long-lasting. 3 The hyperpolarizing responses to these agents were not affected by indomethacin or $N^{G}$–nitro-L-arginine (L-NOARG). 4 In $Ca^{2+}$–free medium, neither TSG nor CPA elicited hyperpolarization, in contrast to acetylcholine which generated a transient hyperpolarizing response. 5 In rings of mesenteric artery precontracted with phenylephrine, TSG and CPA produced endothelium-dependent relaxations. L-NOARG significantly inhibited the relaxations to these agents, but about 40–60% of the total relaxation was resistant to L-NOARG. The L-NOARG-resistant relaxations were abolished by potassium depolarization. 6 These results indicate that TSG and CPA can cause endothelium-dependent hyperpolarization in rat mesenteric artery possibly by releasing endothelium-derived hyperpolarizing factor and that membrane hyperpolarization can contribute to the endothelium-dependent relaxations to these agents. The mechanism of hyperpolarization may be related to increased $Ca^{2+}$ influx into endothelial cells triggered by depletion of intracellular $Ca^{2+}$ stores due to inhibition of endoplasmic reticulum $Ca^{2+}$–pump ATPase activity. |
| Related Links | http://europepmc.org/articles/pmc1909013?pdf=render https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1476-5381.1995.tb15908.x |
| Ending Page | 992 |
| Page Count | 6 |
| Starting Page | 987 |
| e-ISSN | 14765381 |
| DOI | 10.1111/j.1476-5381.1995.tb15908.x |
| Journal | British Journal of Pharmacology |
| Issue Number | 6 |
| Volume Number | 115 |
| Language | English |
| Publisher | Wiley-Blackwell |
| Publisher Date | 1995-07-19 |
| Access Restriction | Open |
| Subject Keyword | Journal: British Journal of Pharmacology Cyclopiazonic Acid Hyperpolarization Vascular Smooth Muscle |
| Content Type | Text |
| Resource Type | Article |
