Irbesartan-mediated AT receptor blockade attenuates hyposmotic-induced enhancement of current and prevents shortening of action potential duration in atrial myocytes
Introduction: Stretch of the atrial membrane upregulates the slow component of delayed rectifier K + current ( I Ks ). Blockade of angiotensin II subtype 1 receptors (AT 1 R) attenuates this increase in I Ks . The present study aimed to examine the effects of irbesartan, a selective AT 1 R blocker (...
| Main Authors: | , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
SAGE Publications
2014-12-01
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| Series: | Journal of the Renin-Angiotensin-Aldosterone System |
| Online Access: | https://doi.org/10.1177/1470320312474855 |
| Summary: | Introduction: Stretch of the atrial membrane upregulates the slow component of delayed rectifier K + current ( I Ks ). Blockade of angiotensin II subtype 1 receptors (AT 1 R) attenuates this increase in I Ks . The present study aimed to examine the effects of irbesartan, a selective AT 1 R blocker (ABR), on both the enhancement of I Ks and the shortening of action potential duration (APD) induced by stretching atrial myocytes for exploring the mechanisms underlying the prevention of atrial fibrillation (AF) by ABR. Methods: Hyposmotic solution (Hypo-S) was used to stretch guinea pig atrial myocytes. I Ks and APD were recorded using the whole-cell patch-clamp technique. Results: Irbesartan (1–50 μM) attenuated the Hypo-S-induced increase in I Ks and shortening of APD 90 . Hypo-S increased the I Ks by 113.4%, whereas Hypo-S + 1 μM irbesartan and Hypo-S + 50 μM irbesartan increased the I Ks by only 74.5% and 70.3%, respectively. In addition, Hypo-S shortened the APD 90 by 19.0%, whereas Hypo-S + 1 μM irbesartan and Hypo-S + 50 μM irbesartan shortened the APD 90 by 12.1% and 12.0%, respectively. Conclusion: The actions of irbesartan on electrical changes induced by stretching atrial myocytes are associated with blocking AT 1 R. These actions may be beneficial for treating AF. |
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| ISSN: | 1470-3203 1752-8976 |