Valsartan-induced cardioprotection involves angiotensin II type 2 receptor upregulation in isolated ischaemia and reperfused rat hearts
| Autor: | Ke-yan Li, Ying-jie Zhang |
|---|---|
| Rok vydání: | 2015 |
| Předmět: |
Male
Angiotensin receptor medicine.medical_specialty Blotting Western Tetrazoles Myocardial Reperfusion Injury Real-Time Polymerase Chain Reaction Receptor Angiotensin Type 2 Rats Sprague-Dawley Internal medicine Coronary Circulation medicine Animals cardiovascular diseases RNA Messenger Receptor Cardioprotection Angiotensin II receptor type 1 biology business.industry Valine General Medicine Angiotensin II Rats Up-Regulation Disease Models Animal Endocrinology Valsartan Gene Expression Regulation cardiovascular system biology.protein Ventricular pressure Cardiology Creatine kinase Cardiology and Cardiovascular Medicine business Angiotensin II Type 1 Receptor Blockers medicine.drug |
| Zdroj: | Acta cardiologica. 70(1) |
| ISSN: | 0001-5385 |
| Popis: | The angiotensin II type 1 receptor (AT1R) antagonist protects the heart against acute ischaemia-reperfusion injury. The underlying mechanism is unclear. To determine the effects of angiotensin II type 1 receptor blockade, valsartan on AT1 and AT2 receptor during ischaemia reperfusion in isolated rat, the hearts of 24 SD rats were isolated, linked to Langendorff perfusion apparatus, and exposed to ischaemia for 30 min.The left ventricular systolic pressure, maximal uprising velocity of left ventricular pressure (+dp/dt(max)), maximal decreasing velocity of left ventricular pressure (-dp/dt(max)) and coronary flow were measured after stabilization of the perfusion.The isoenzyme of creatine kinase in the effluent liquid from the heart, AT1 and AT2 receptor mRNA and protein expression were measured after stabilization of the perfusion. The results showed that ischaemia-reperfusion induced a marked decrease in left ventricular systolic pressure, +dp/dt(max) and -dp/dt(max) indicating severe cardiac dysfunction and decreased coronary effluence. Concurrently, myocardial AT1 and AT2 receptor mRNA and protein expression were increased with valsartan. However, AT2 receptor mRNA and protein expression decreased during ischaemia-reperfusion. The creatine kinase levels at different time points of the valsartan group were significantly lower. The results suggested that valsartan improved left ventricular function and increased coronary effluence because the angiotensin receptor blocker valsartan induced cardioprotection associated with upregulating AT2 receptor protein and mRNA expression after ischaemia-reperfusion in isolated rats. |
| Databáze: | OpenAIRE |
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