Effects of ramipril on cardiac gene transcription levels of angiotensin II receptors after myocardial infarction
Abstract
AIM:
To study the early changes of cardiac angiotensin (Ang) II receptor gene transcription after myocardial infarction (MI) in rats chronically treated with the angiotensin-converting enzyme (ACE) inhibitor ramipril.
METHODS:
MI was induced by left anterior descending coronary artery ligation in rats and sham-operated rats were used as control. Rats were treated daily with ramipril (1 mg.kg-1) or water, initiated 1 wk before surgery. Quantitative RT-PCR was applied to determine the Ang II receptors AT1, AT2 receptor gene mRNA levels in the non-infarcted myocardium.
RESULTS:
AT1 and AT2 mRNA levels increased time point-dependently in the cardiac septum after MI reaching a peak on d 1. There was no significant difference of the myocardial AT1 and AT2 receptor mRNA levels between the ramipril-treated and water-treated rats after MI.
CONCLUSION:
The AT1 and AT2 receptor gene transcription in the non-infarcted myocardium was associated with the process of cardiac remodeling after MI but not affected by ACE inhibition.
Keywords:
To study the early changes of cardiac angiotensin (Ang) II receptor gene transcription after myocardial infarction (MI) in rats chronically treated with the angiotensin-converting enzyme (ACE) inhibitor ramipril.
METHODS:
MI was induced by left anterior descending coronary artery ligation in rats and sham-operated rats were used as control. Rats were treated daily with ramipril (1 mg.kg-1) or water, initiated 1 wk before surgery. Quantitative RT-PCR was applied to determine the Ang II receptors AT1, AT2 receptor gene mRNA levels in the non-infarcted myocardium.
RESULTS:
AT1 and AT2 mRNA levels increased time point-dependently in the cardiac septum after MI reaching a peak on d 1. There was no significant difference of the myocardial AT1 and AT2 receptor mRNA levels between the ramipril-treated and water-treated rats after MI.
CONCLUSION:
The AT1 and AT2 receptor gene transcription in the non-infarcted myocardium was associated with the process of cardiac remodeling after MI but not affected by ACE inhibition.