Abstract
BackgroundStress-induced cardiomyopathy (SIC) has gained increasing attention worldwide and is characterized by extensive ventricular akinesis, Beta-blockers and angiotensin-converting enzyme inhibitors (ACEIs) are the main treatments for SIC patients. The pharmacological mechanism of action of beta-blockers results in the inhibition of the biological effects of catecholamines. However, the mechanism of action of ACEIs in the treatment of cardiomyopathy is not known. Our aim is to assess changes in levels of angiotensin II, angiotensin-II receptors and ACE responses to SIC.MethodsA model of inverted SIC was established in rabbits by vagal electrical stimulation. The serum concentration of angiotensin II and angiotensin (1-7) was detected by enzyme-linked immunosorbent assay. Expression of angiotensin-II receptors was measured by Western blotting and real-time reverse transcription-polymerase chain reaction (RT-PCR), with localization detected by immunofluorescent staining. ACE-II expression in the myocardium was measured by Western blotting.ResultsFrom one day after vagal stimulation, concentrations of angiotensin II were significantly higher in the experimental group than those in the control group (P <0.05). Stress induced a time-dependent decrease in angiotensin subtype-1 (AT1) expression and a time-dependent increase in AT2 expression only in the apical portion of the myocardium. From three days after vagal stimulation, angiotensin (1-7) levels were significantly lower in the experimental group compared with the control group (P <0.05). Expression of the ACE-II protein was significantly downregulated in the experimental group compared with the control group from three days after vagal stimulation (P <0.05).ConclusionsExpression of angiotensin II, its receptors, ACE-II and angiotensin (1-7) was altered in response to SIC. The renin-angiotensin system could represent a therapeutic target in the prevention of SIC.Electronic supplementary materialThe online version of this article (doi:10.1186/s40001-014-0054-8) contains supplementary material, which is available to authorized users.
Highlights
Stress-induced cardiomyopathy (SIC) has gained increasing attention worldwide and is characterized by extensive ventricular akinesis, Beta-blockers and angiotensin-converting enzyme inhibitors (ACEIs) are the main treatments for SIC patients
Change in plasma levels of angiotensin II in response to stress At 0, 1, 3, 7 and 14 days after vagal stimulation, the plasma of rabbits in control and experimental groups was extracted, and the concentration of angiotensin II measured by enzyme-linked immunoassay (ELISA)
The concentrations of angiotensin II were significantly higher in experimental group than those in the control group from one day after vagal stimulation (P
Summary
Stress-induced cardiomyopathy (SIC) has gained increasing attention worldwide and is characterized by extensive ventricular akinesis, Beta-blockers and angiotensin-converting enzyme inhibitors (ACEIs) are the main treatments for SIC patients. Beta-blockers and angiotensinconverting enzyme inhibitors (ACEIs) are the main treatments for SIC patients [3, 7, 8]. The pharmacological mechanism of action of beta-blockers results in the inhibition of the biological effects of catecholamines [9]. The target of ACEIs is angiotensin-converting enzyme 1 (the main function of which is to convert angiotensinogen to angiotensin II). Angiotensin II activates several nuclear transcription factors (such as signal transducer and activator of transcription (STAT) and cyclic adenosine monophosphate (cAMP) response element-binding (CREB) protein) by promoting fibroblast proliferation that leads to myocardial remodeling [12,13]
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