scholarly journals Cardioprotective Effects of Qishenyiqi Mediated by Angiotensin II Type 1 Receptor Blockade and Enhancing Angiotensin-Converting Enzyme 2

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Yong Wang ◽  
Chun Li ◽  
Yulin Ouyang ◽  
Junda Yu ◽  
Shuzhen Guo ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ejection Fraction ◽  
Ace Inhibitor ◽  
Left Ventricular ◽  
Myocardial Tissue ◽  
Receptor Blockade ◽  
Converting Enzyme ◽  
Angiotensin Converting Enzyme 2 ◽  
Cardioprotective Effects

The aim of this paper was to investigate whether the effects of QSYQ on CHD are associated with the renin-angiotensin-aldosterone system (RAAS). The formula groups were lavaged with QSYQ, using fosinopril sodium as a control. The level of RAAS components in the myocardial tissue was measured, respectively. The results showed that both QSYQ and fosinopril sodium can improve the ejection fraction in CHD and that QSYQ decreases the left ventricular end-systolic diameter and left ventricular end-diastolic diameter, while fosinopril sodium has no effects on these parameters. Fosinopril sodium, as an ACE inhibitor, downregulated ACE expression and eventually reduced the tissue AngII concentration but had no effect on ACE2. Moreover, it had no effect on renin or AT2, while QSYQ significantly decreased the level of renin and expression of AngII in myocardial tissue. The results also revealed that QSYQ can act on both AT1 and AT2, thus, blocking the effect of AngII and increasing the level of ACE2. It also downregulated the levels of TGF-βand MMP-9, but it had no effect on ACE. This study showed that the ameliorative effects of QSYQ on CHD in rats had multiple targets associated with the inhibition of RAAS, thus, producing cardioprotective therapy effects.

Abstract 14401: Elevated Levels of Angiotensin II Type 1 Receptor Autoantibodies Are Associated With Abnormal Echocardiogram Parameters in Women With Preeclampsia

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Anum S Minhas ◽  
Sammy Zakaria ◽  
Monica Mukherjee ◽  
Theresa Boyer ◽  
Neal Fedarko ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Ejection Fraction ◽  
Systolic Function ◽  
Clinical Manifestations ◽  
Left Ventricular ◽  
Lv Remodeling ◽  
Echocardiographic Parameters ◽  
Prospective Longitudinal

Introduction: Preeclampsia (PEC) increases the long-term risk for heart failure with preserved ejection fraction (HFpEF). While the underlying pathogenesis is unknown, angiotensin II type 1 receptor autoantibodies (AT1-AA) have been implicated. AT1-AA bind agonistically to the AT1 receptor and may result in clinical manifestations of preeclampsia. We aimed to determine whether women with PEC have elevated AT1-AA levels compared to normotensive women (controls) during pregnancy and at 4 years postpartum, and whether AT1-AA levels correlate with abnormal echocardiographic parameters. Methods: We performed a prospective longitudinal cohort study comparing women with PEC (n=21) to controls (n=20). AT1-AA and echocardiographic measurements were obtained during pregnancy and 4 years postpartum. Linear regression analyses were performed to evaluate the association between AT1-AA levels and important echocardiographic parameters. Results: Mean AT1-AA level during pregnancy differed significantly between women with PEC versus healthy pregnant controls (10.21±3.20 vs 6.33±3.40 μg/ml, p<0.001). Women with PEC were more likely to be black and deliver at an earlier gestational age. Higher AT1-AA was associated with increased systolic/diastolic blood pressure, echocardiographic markers of biventricular systolic function (tricuspid annular systolic plane excursion and left ventricular (LV) ejection fraction), concentric LV hypertrophy and worsened diastolic function. AT1-AA remained persistently elevated at 4 years in women with PEC at baseline compared to controls (12.76±5.13 vs 4.47±1.49 μg/ml, p<0.001) (Figure 1). Conclusions: Women with PEC have elevated AT1-AA compared to controls, both during pregnancy and 4 years postpartum. Higher AT1-AA is associated with abnormal diastolic parameters, LV remodeling, and hyperdynamic biventricular function. These findings suggest that AT1-AA plays an important role in the risk of HFpEF in PEC.

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