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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >The ability of phosphodiesterase-5 inhibitors sildenafil and ordonafil to reverse L-NAME induced cardiac hypertrophy in the rabbit: Possible role of calcineurin and p38
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The ability of phosphodiesterase-5 inhibitors sildenafil and ordonafil to reverse L-NAME induced cardiac hypertrophy in the rabbit: Possible role of calcineurin and p38

机译：磷酸二酯酶5抑制剂西地那非和奥多那非逆转L-NAME引起的兔心脏肥大的能力：钙​​调磷酸酶和p38的可能作用

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摘要

Phosphodiesterase 5 inhibitors (PDE-5Is) can suppress and (or) reverse pressure overload induced myocardial hypertrophy. This study investigated the suppressive effect of 2 PDE-5Is (sildenafil and ordonafil) on N-nitro-L-arginine methyl ester (L-NAME)-induced cardiac hypertrophy in rabbit heart, and examined their possible mechanism of action. L-NAME increased left ventricular thickness to 6.1± 0.18 mm from 4.6 ± 0.13 mm (p 0.05), which regressed after treatment with either sildenafil or or-donafil to 5.1 ± 0.1 mm and 4.8 ± 0.2 mm, respectively (p 0.05). Phenylephrine increased neonatal rat ventricular myocyte cell surface area to 131% ± 3% of the control value, which was associated with significant increment in ERK1/2 to 143% ± 5% of the control value (p 0.05). Ordonafil and sildenafil decreased cell surface area to 95% ± 3% and 90% ± 1% of the control value, respectively. Both drugs decreased ERK1/2 to 88% ± 4% of the control value. Calcineurin activity was significantly decreased after 1 h of treatment with 0.1 mg·L -1 ordonafil (1.15 ± 0.05, p 0.05). For sildenafil (0.1 mg·L -1), calcineurin activity significantly decreased only after 24 h of incubation (22%). Also p38 activation was attenuated by ordonafil and sildenafil (0.1 mg·L -1). It is suggested that both drugs have the ability to reverse L-NAME-induced cardiac hypertrophy and suppress phenylphrine-induced myocyte hypertrophy, and that these effects may be mediated through the attenuation of calcineurin and its downstream signaling pathways (p38) in neonatal rat ventricular myocytes.
机译：磷酸二酯酶5抑制剂（PDE-5Is）可以抑制和（或）逆转压力超负荷引起的心肌肥大。这项研究调查了2种PDE-5Is（西地那非和奥多那非）对N-硝基-L-精氨酸甲酯（L-NAME）引起的兔心脏肥大的抑制作用，并研究了其可能的作用机理。 L-NAME将左心室厚度从4.6±0.13毫米增加到6.1±0.18毫米（p <0.05），西地那非或奥达那非治疗后分别回归至5.1±0.1毫米和4.8±0.2毫米（p <0.05 ）。苯肾上腺素使新生大鼠心室肌细胞表面积增加至对照值的131％±3％，这与ERK1 / 2的显着增加至对照值的143％±5％有关（p <0.05）。奥多那非和西地那非分别将细胞表面积降低至对照值的95％±3％和90％±1％。两种药物的ERK1 / 2均降至对照值的88％±4％。用0.1 mg·L -1奥多那非治疗1 h后，钙调神经磷酸酶活性显着降低（1.15±0.05，p <0.05）。西地那非（0.1 mg·L -1）的钙调神经磷酸酶活性仅在孵育24小时后才显着下降（22％）。奥多那非和西地那非（0.1 mg·L -1）也会减弱p38的激活。提示这两种药物都具有逆转L-NAME引起的心脏肥大和抑制苯肾上腺素引起的心肌细胞肥大的能力，并且这些作用可能通过降低钙调神经磷酸酶及其下游信号通路（p38）介导。肌细胞。

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