Reversal of angiotensin-(1-12)-caused positive modulation on left ventricular contractile performance in heart failure: Assessment by pressure-volume analysis.
Reversal of angiotensin-(1-12)-caused positive modulation on left ventricular contractile performance in heart failure: Assessment by pressure-volume analysis.
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血管紧张素（1-12）的逆转导致心力衰竭左心室收缩性能的正向调节：通过压力-容量分析进行评估
DOI：
10.1016/j.ijcard.2019.09.004
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发表时间：
2020-02-15
影响因子：
3.5
通讯作者：
Cheng CP
中科院分区：
文献类型：
--
作者：
Li T;Zhang Z;Zhang X;Chen Z;Cheng HJ;Ahmad S;Ferrario CM;Cheng CP
血管紧张素-（1-12）[Ang-（1-12）]是由糜酶直接产生血管紧张素-II的非肾素依赖性前体。大量证据表明，心力衰竭（HF）可能会改变心脏Ang-（1-12）的表达和活性;这种新的Ang-（1-12）/糜酶轴可能是HF中血管紧张素II有害作用的主要来源。我们假设HF改变心脏对Ang-（1-12）的反应。它的刺激可产生心脏负性调制，加重左心室（LV）收缩和舒张功能障碍。我们在16只SD雄性大鼠中评估了Ang-（1-12）（2 nmol/kg/min，iv，10 min）对异丙肾上腺素诱导的HF（170 mg/kg sq.连续2天）和10名年龄匹配的男性对照。在正常对照组中，与基线相比，Ang-（1-12）增加LV收缩末期压，而不改变心率、动脉弹性（EA）、LV舒张末期压（PED）、时间常数（τ）和射血分数（EF）。Ang-（1-12）显著增加压力（P）-容积（V）关系的斜率（EES和MSW），表明LV收缩力增加。AVC（量化为EES/EA）改善。相比之下，在HF中，与HF基线相比，Ang-（1-12）产生类似的PES增加，但显著增加τ、EA和PED。左室舒张早期P-V环上移，EF降低。此外，Ang-（1-12）显著降低EES和MSW，表明LV收缩力降低。AVC下降了43%。在正常和HF大鼠中，Ang-（1-12）引起相似的血管收缩。在正常情况下，Ang-（1-12）增加LV收缩功能。在心力衰竭中，Ang-（1-12）具有不良影响，并抑制LV收缩和舒张功能性能。
Angiotensin-(1–12) [Ang-(1–12)] is a renin-independent precursor for direct angiotensin-II production by chymase. Substantial evidence suggests that heart failure (HF) may alter cardiac Ang-(1–12) expression and activity; this novel Ang-(1–12)/chymase axis may be the main source for angiotensin-II deleterious actions in HF. We hypothesized that HF alters cardiac response to Ang-(1–12). Its stimulation may produce cardiac negative modulation and exacerbate left ventricle (LV) systolic and diastolic dysfunction. We assessed the effects of Ang-(1–12) (2 nmol/kg/min, iv, 10 min) on LV contractility, LV diastolic filling, LV-arterial coupling (AVC) in 16 SD male rats with HF-induced by isoproterenol (3 mo after 170 mg/kg sq. for 2 consecutive days) and 10 age-matched male controls. In normal controls, versus baseline, Ang-(1–12) increased LV end-systolic pressure, without altering heart rate, arterial elastance (EA), LV end-diastolic pressure (PED), the time constant (τ) and ejection fraction (EF). Ang-(1–12) significantly increased the slopes (EES and MSW) of pressure (P)-volume (V) relations, indicating increased LV contractility. AVC (quantified as EES/EA) improved. In contrast, in HF, versus HF baseline, Ang-(1–12) produced a similar increase in PES, but significantly increased τ, EA, and PED. The early diastolic portion of LV P-V loop was shifted upward with reduced in EF. Moreover, Ang-(1–12) significantly decreased EES and MSW, demonstrating decreased LV contractility. AVC was decreased by 43%. In both normal and HF rats, Ang-(1–12) causes similar vasoconstriction. In normal, Ang-(1–12) increases LV contractile function. In HF, Ang-(1–12) has adverse effects and depresses LV systolic and diastolic functional performance.
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DOI：
10.1042/cs20130400
发表时间：
2014-04
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Ferrario CM;Ahmad S;Nagata S;Simington SW;Varagic J;Kon N;Dell'italia LJ
通讯作者：
Dell'italia LJ
影响因子：
15.9
作者：
DellItalia, LJ;Meng, QC;Oparil, S
通讯作者：
Oparil, S
影响因子：
37.8
作者：
Cheng, Che-Ping;Cheng, Heng-Jie;Little, William C.
通讯作者：
Little, William C.
影响因子：
3.7
作者：
Grimm, D;Holmer, SR;Kromer, EP
通讯作者：
Kromer, EP
影响因子：
3.7
作者：
Ahmad S;Simmons T;Varagic J;Moniwa N;Chappell MC;Ferrario CM
通讯作者：
Ferrario CM