Altered norepinephrine content and ventricular function in p75NTR-/- mice after myocardial infarction.
Altered norepinephrine content and ventricular function in p75NTR-/- mice after myocardial infarction.
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DOI：
10.1016/j.autneu.2011.05.002
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发表时间：
2011-10-28
影响因子：
2.7
通讯作者：
Habecker, Beth A.
中科院分区：
文献类型：
--
作者：
Lorentz, Christina U.;Woodward, William R.;Tharp, Kevin;Habecker, Beth A.
心脏交感神经元通过释放去甲肾上腺素刺激心率和收缩力。神经生长因子通过激活TrkA和p75NTR调节交感神经传递。神经生长因子在梗死后交感神经重构中起重要作用。我们使用缺乏p75NTR的小鼠来研究心肌梗死后神经生长因子信号传导改变对交感神经肽表达、心脏去甲肾上腺素和心室功能的影响。缺血再灌注手术后，野生型和p75 NTR −/−小鼠的脑梗死面积相似。同样，编码血管活性肠肽、甘丙肽和垂体腺苷酸环化酶激活肽的mRNA在野生型和p75 NTR −/−心脏交感神经元中是相同的，TrkA神经营养因子受体的表达也是相同的。与野生型相比，p75 NTR −/−心室底部的去甲肾上腺素含量升高，但闭塞部位以下的水平相同。术后3天和7天在异氟醚麻醉下测量左心室压力、dP/dtMAX和dP/dtMIN。心肌梗死后3天心室压显著下降，多巴酚丁胺刺激β受体和酪胺释放内源性去甲肾上腺素显示dP/dtMAX不足。dP/dtMIN不受基因型或手术组的影响。手术后3天，在基因型之间观察到很少的差异，与先前在对照p75 NTR −/−动物中报道的低压和dP/dtMAX相反。术后7天，p75 NTR −/−心脏的心室压和dP/dtMAX显著低于WT心脏。因此，p75NTR的缺乏并没有增强心肌梗死后的心功能。
Cardiac sympathetic neurons stimulate heart rate and the force of contraction through release of norepinephrine. Nerve growth factor modulates sympathetic transmission through activation of TrkA and p75NTR. Nerve growth factor plays an important role in post-infarct sympathetic remodeling. We used mice lacking p75NTR to examine the effect of altered nerve growth factor signaling on sympathetic neuropeptide expression, cardiac norepinephrine, and ventricular function after myocardial infarction. Infarct size was similar in wildtype and p75NTR−/− mice after ischemia-reperfusion surgery. Likewise, mRNAs encoding vasoactive intestinal peptide, galanin, and pituitary adenylate cyclase activating peptides were identical in wildtype and p75NTR−/− cardiac sympathetic neurons, as was expression of the TrkA neurotrophin receptor. Norepinephrine content was elevated in the base of the p75NTR−/− ventricle compared to wildtype, but levels were identical below the site of occlusion. Left ventricular pressure, dP/dtMAX, and dP/dtMIN were measured under isoflurane anesthesia 3 and 7 days after surgery. Ventricular pressure decreased significantly 3 days after infarction, and deficits in dP/dtMAX were revealed by stimulating beta receptors with dobutamine and release of endogenous norepinephrine with tyramine. dP/dtMIN was not altered by genotype or surgical group. Few differences were observed between genotypes 3 days after surgery, in contrast to low pressure and dP/dtMAX previously reported in control p75NTR−/− animals. Seven days after surgery ventricular pressure and dP/dtMAX were significantly lower in p75NTR−/− hearts compared to WT hearts. Thus, the lack of p75NTR did not enhance cardiac function after myocardial infarction.
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影响因子：
2.9
作者：
Alston EN;Parrish DC;Hasan W;Tharp K;Pahlmeyer L;Habecker BA
通讯作者：
Habecker BA
影响因子：
3.4
作者：
Hannila, SS;Lawrance, GM;Kawaja, MD
通讯作者：
Kawaja, MD
影响因子：
37.8
作者：
Graham, LN;Smith, PA;Mary, DASG
通讯作者：
Mary, DASG
DOI：
10.1152/ajpheart.00749.2007
发表时间：
2008-03-01
影响因子：
4.8
作者：
Huang, Ruiping;Karve, Amrita;Abela, George S.
通讯作者：
Abela, George S.
影响因子：
3
作者：
Gasz, B;Rácz, B;Reglodi, D
通讯作者：
Reglodi, D