Regulation of angiotensin II receptors on ventricular myocytes after myocardial infarction in rats.
Regulation of angiotensin II receptors on ventricular myocytes after myocardial infarction in rats.
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DOI：
10.1161/01.res.72.6.1149
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发表时间：
1993-06
影响因子：
20.1
通讯作者：
L. Meggs;J. Coupet;Harer Huang;W. Cheng;Peng Li;J. Capasso;J. Homcy;P. Anversa
中科院分区：
文献类型：
--
作者：
L. Meggs;J. Coupet;Harer Huang;W. Cheng;Peng Li;J. Capasso;J. Homcy;P. Anversa
为确定急性心肌梗死对血管紧张素II （Ang II）受体调节及左右心室肌细胞收缩性能的影响，采用手术诱导大鼠冠状动脉结扎，1周后检测Ang II受体密度、亲和力及存活肌细胞力学性能。心脏泵功能的生理测定揭示了心室衰竭的存在，这在细胞水平上与心肌细胞缩短和再延长速度的降低、达到峰值缩短的时间延长以及细胞缩短程度的降低有关。这些单细胞功能异常在左心室肌细胞中比在右心室肌细胞中更为突出。细胞肥大的记录是细胞长度和宽度的增加，在梗死左心室的备用肌细胞中也更大。反应性肥大伴随着左右肌细胞Ang II受体密度分别增加1.84倍和1.85倍。另一方面，Ang II受体对放射性标记拮抗剂的亲和力没有改变。然而，在梗死后，Ang ii刺激的左肌细胞和右肌细胞的磷酸肌醇周转分别增加了3.7倍和2.5倍。发现心室肌细胞只具有AT1受体亚型。综上所述，心肌梗死导致剩余细胞的收缩行为受损，并激活Ang II受体及其相关的效应通路，这可能与活细胞的反应性生长适应有关。
To determine the effects of acute myocardial infarction on the regulation of angiotensin II (Ang II) receptors and contractile performance of left and right ventricular myocytes, coronary artery ligation was surgically induced in rats, and Ang II receptor density and affinity and the mechanical properties of surviving muscle cells were examined 1 week later. Physiological determinations of cardiac pump function revealed the presence of ventricular failure, which was associated at the cellular level with a depression in the velocity of myocyte shortening and relengthening, a prolongation of time to peak shortening, and a reduction in the extent of cell shortening. These abnormalities in single-cell function were more prominent in left than in right ventricular myocytes. Cellular hypertrophy was documented by increases in cell length and width, which were also greater in the spared myocytes of the infarcted left ventricle. Reactive hypertrophy was accompanied by a 1.84- and 1.85-fold increase in the density of Ang II receptors on left and right myocytes, respectively. On the other hand, the affinity of Ang II receptors for the radiolabeled antagonist was not altered. However, Ang II-stimulated phosphoinositol turnover was enhanced by 3.7- and 2.5-fold in left and right myocytes, respectively, after infarction. Ventricular myocytes were found to possess the AT1 receptor subtype exclusively. In conclusion, myocardial infarction leads to impairment in the contractile behavior of the remaining cells and to the activation of Ang II receptors and effector pathway associated with these receptors, which may be involved in the reactive growth adaptation of the viable myocytes.