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| Content Provider | Springer Nature Link |
|---|---|
| Author | Matsuda, Hiroyuki Kurata, Yasutaka Imanishi, Sunao Sato, Ryoichi Shibamoto, Toshishige |
| Copyright Year | 2004 |
| Abstract | We investigated the effects of angiotensin II (Ang II) on the sustained outward current (I sus) and action potential of rat ventricular myocytes using the whole-cell patch-clamp technique. Ang II at 30 nM~3 µM inhibited I sus with an IC50 of 240 nM, a Hill coefficient of 1.0 and maximum inhibition of 19.4%. Ang II-mediated inhibition of I sus was voltage independent, was due to a decrease in the K+ current and was abolished by the Ang II type-I (AT1) receptor blocker, valsartan. The protein kinase C (PKC) inhibitors PKC19–36 or calphostin C, abolished Ang II-mediated inhibition of I sus. In contrast, pretreatment with the protein kinase A (PKA) inhibitor PKA6–22 (100 µM) significantly enhanced the suppression of I sus by 1 µM Ang II: (33.7±5.1% vs. control 17.1±2.3%). These results indicate that Ang II inhibits I sus via the AT1 receptor and activation of PKC. Ang II significantly prolonged action potential duration (APD) when the control APD was lengthened by a Ca2+ channel activator, BAY K8644. In myocytes with a relatively long APD, Ang II may prolong APD by inhibiting I sus. |
| Starting Page | 54 |
| Ending Page | 62 |
| Page Count | 9 |
| File Format | |
| ISSN | 00316768 |
| Journal | Pflügers Archiv |
| Volume Number | 448 |
| Issue Number | 1 |
| e-ISSN | 14322013 |
| Language | English |
| Publisher | Springer-Verlag |
| Publisher Date | 2003-12-18 |
| Publisher Place | Berlin, Heidelberg |
| Access Restriction | One Nation One Subscription (ONOS) |
| Subject Keyword | Angiotensin II Sustained outward current Angiotensin II type-1 receptor Protein kinase C Rat ventricular myocyte |
| Content Type | Text |
| Resource Type | Article |
| Subject | Physiology Physiology (medical) Clinical Biochemistry |
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