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• W2023521188 abstract "Recent evidence indicates that Angiotensin (A)-(1-7) plays a key role in the maintenance of cardiac function. However, the exact means by which A-(1-7) affords cardioprotection are unclear, and its direct effect on cardiac contractility remains to be determined. We previously demonstrated that in heart failure (HF), Angiotensin II (AII) decreases left ventricle (LV) contractility. A-(1-7) may antagonize AII-induced cardiac depression, thereby contributing to the beneficial actions in HF. We assessed the hypothesis that A-(1-7) may produce positive modulation on Ca2+ current (ICa,L) and increase LV and myocyte contractility via A-(1-7) receptor Mas, acting through nitric oxide (NO)/bradykinin (BK)-mediated mechanism. We measured LV contractility changes after A-(1-7) (650 ng/kg, iv), which produced more than a 20-fold increase in plasma A-(1-7) levels, mimicking the elevations caused by angiotensin-converting enzyme inhibitor in HF patients, and compared myocyte contractile and ICa,L responses to A-(1-7) (10−5 M) in 15 rats with isoproterenol (ISO)-induced HF (3 months after 170 mg/kg sq for 2 days). LV contractility was measured by pressure-volume analysis. ICa,L was measured using whole-cell voltage clamp technique. In additional contractile studies, myocytes were pretreated to inhibit either NO synthase (L-NAME, 10−5 M), BK (HOE 140, 10−6 M) or A-1-7 receptor Mas (A-779 A, 10−5 M) followed with A-(1-7) exposure. Compared with baseline (C), after A-(1-7) (A), EES (41%, A:1.1 vs C: 0.78 mmHg/μl) and Msw (39%, 93.6 vs 67.5 mmHg) were increased, indicating enhanced LV contractility. In HF myocytes, A-(1-7) increased myocyte percent shortening (31%, 7.1% vs 5.4%), the velocity of cell contraction (33%, 108.4 vs 81.4 μm/sec) and relengthening (36%, 73.8 vs 54.3 μm/sec) accompanied by significantly-increased peak ICa,L (24%, 6.3 ± 0.3 vs 5.1 ± 0.2 pA/pF). L-NAME increased, HOE 140 decreased, and A-(1-7) receptor Mas antagonist prevented myocyte contractile and ICa,L responses to A-(1-7). In HF, clinically-relevant concentrations of A-(1-7) counteracted AII-induced cardiac depression, increased ICa,L, and produced positive inotropic effects in both LV and myocytes. These effects are coupled with A-(1-7) receptor Mas and involve activation of NO/BK pathways." @default.
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• W2023521188 date "2011-08-01" @default.
• W2023521188 modified "2023-10-18" @default.
• W2023521188 title "Cellular Basis for Angiotensin-(1-7)-Induced Positive Modulation on Cardiac Contractile Performance in Heart Failure" @default.
• W2023521188 doi "https://doi.org/10.1016/j.cardfail.2011.06.225" @default.
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