Aorta and skeletal muscle NO synthase expression in experimental heart failure
Aorta and skeletal muscle NO synthase expression in experimental heart failure
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DOI：
10.1006/jmcc.1996.0216
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发表时间：
1996-11-01
影响因子：
5
通讯作者：
Ferrari, R
中科院分区：
文献类型：
--
作者：
Comini, L;Bachetti, T;Ferrari, R
一氧化氮（NO）是由NO合酶（NOS）从L-精氨酸合成的自由基，其导致内皮源性舒张因子的生物活性。有证据表明，在充血性心力衰竭（CHF）患者的外周血管中，NO的可用性降低，本研究的目的是研究一氧化氮合酶在心力衰竭大鼠降主动脉和骨骼肌中的表达，野百合碱用于诱导大鼠的肺动脉高压和心力衰竭。通过蛋白质印迹分析评估酶的组成型（ecNOS）和诱导型（iNOS）同种型的表达。在CHF动物中，ecNOS在主动脉中的位置改变：内皮蛋白表达显著降低（从0.083 +/- 0.012至0.003 +/- 0.004 OD/μ g总蛋白，P
Nitric oxide (NO), the free radical that accounts for the biological activity of endothelium-derived relaxing factor, is synthesized from L-arginine by NO synthase (NOS), There is evidence that NO availability is reduced in the peripheral vasculature of patients with congestive heart failure (CHF), The aim of this study was to investigate the expression of NOS in the descending aorta and in the skeletal muscles of rats subjected to heart failure, The alkaloid, monocrotaline, was used to induce pulmonary hypertension and cardiac failure in rats, The expression of both the constitutive (ecNOS) and the inducible (iNOS) isoforms of the enzyme was assessed by Western blot analysis, In CHF animals, the ecNOS location in the aorta is altered: the endothelial protein expression is substantially reduced (from 0.083 +/- 0.012 to 0.003 +/- 0.004 OD/mu g total proteins, P