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The antifibrotic agent pirfenidone inhibits angiotensin II-induced cardiac hypertrophy in mice
TLDR
Results indicate that pirfenidone might be effective as an antifibrotic drug in the treatment of cardiac hypertrophy induced by hypertension. Expand
Tolvaptan Improves Left Ventricular Dysfunction after Myocardial Infarction in Rats
TLDR
Tolvaptan may improve cardiac dysfunction after MI, which is partially mediated by the suppression of V1a receptor, neurohumoral activation and inflammation. Expand
Effects of exogenous big endothelin-1 on postischemic cardiac dysfunction and norepinephrine overflow in rat hearts
TLDR
It is suggested that exogenous big ET-1 has beneficial effects on ischemia/reperfusion-induced cardiac injury and it seems likely that bigET-1 is converted to Et-1, locally in the heart, and this ET- 1 preferentially binds to ETB receptors to exert its related beneficial actions. Expand
Sex Differences in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Heart: The Role of Estrogen Against Myocardial Ischemia–reperfusion Damage Via an NO-mediated Mechanism
TLDR
It is suggested that estrogen plays a key role in the cardioprotective effect against I/R injury in female rats, by suppressing NE release via the enhancement of NO production. Expand
Percutaneous carbon dioxide treatment using a gas mist generator enhances the collateral blood flow in the ischemic hindlimb.
TLDR
Percutaneous CO2 mist therapy may be useful for treating ischemia-induced angiogenesis in a mouse ischemic hindlimb model. Expand
Postconditioning Improves Postischemic Cardiac Dysfunction Independently of Norepinephrine Overflow After Reperfusion in Rat Hearts: Comparison With Preconditioning
TLDR
Findings indicate that the beneficial effect of postC on I/R-induced cardiac dysfunction depends on nitric oxide and is irrelevant to NE overflow after reperfusion in contrast to the preC effect. Expand
Protective effects of 17beta-estradiol on post-ischemic cardiac dysfunction and norepinephrine overflow through the non-genomic estrogen receptor/nitric oxide-mediated pathway in the rat heart.
TLDR
The findings suggest that 17β-estradiol exerts cardioprotective effects against ischemia/reperfusion-induced cardiac dysfunction, at least in part, by suppressing norepinephrine overflow, and that nitric oxide production via estrogen receptor activation plays a key role in this process. Expand
Contribution of Nitric Oxide in Big Endothelin-1–induced Cardioprotective Effects on Ischemia/Reperfusion Injury in Rat Hearts
TLDR
The findings suggest that NO produced by ETB receptor activation plays an important role in exogenous big ET-1-induced actions. Expand
Different Effects of AT1 Receptor Antagonist and ETA Receptor Antagonist on Ischemia-Induced Norepinephrine Release in Rat Hearts
TLDR
It is suggested that ETAR antagonist may be more useful than AT1R antagonist in the clinical settings of ischemic heart disease because of its ability to inhibit the exocytotic NE release, but the carrier-mediated NE release induced by prolonged ischemia cannot be avoided by AT2R antagonist. Expand
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