Interaction of myocytes and nonmyocytes is necessary for mechanical stretch to induce ANP/BNP production in cardiocyte culture
Interaction of myocytes and nonmyocytes is necessary for mechanical stretch to induce ANP/BNP production in cardiocyte culture
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DOI：
10.1097/00005344-199800001-00100
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发表时间：
1998-01-01
影响因子：
3
通讯作者：
Nakao, K
中科院分区：
文献类型：
--
作者：
Harada, M;Saito, Y;Nakao, K
在心肌肥大或心室重塑中，同时观察到肌细胞增大和间质或血管周围纤维化，这表明心肌细胞和成纤维细胞之间的相互作用。在这项研究中，我们研究了周期性机械牵张诱导的心肌细胞肥大的机制，重点是心肌细胞和心脏非肌细胞，主要是成纤维细胞之间的相互作用。用Percoll梯度离心法分离新生大鼠心室肌细胞（MC）和非心肌细胞（NMCs），制备心肌细胞原代培养物。当MCs与NMCs共培养时，MCs的体积和ANP/BNP的分泌均显著增加。内皮素-A（ETA）受体拮抗剂BQ-123可显著抑制共培养MC的这种肥大变化。周期性牵张不诱导MC培养的肥大反应。然而，它进一步增加了MC-NMC共培养物中的ANP/BNP产生（在48小时孵育后与非拉伸组相比增加了2.2倍和2.1倍）。在共培养中ANP/BNP产生的这种增加被CV-11974显著抑制，CV-11974是一种血管紧张素H（Ang II）1型受体拮抗剂。这项研究提出了一种可能性，即NMCs通过分泌内皮素-1调节心肌细胞肥大，并且Ang II参与了心肌细胞对机械牵张的肥大反应过程中MCs和NMCs之间的相互作用。
In cardiac hypertrophy or ventricular remodeling, enlargement of myocytes and interstitial or perivascular fibrosis are observed simultaneously, which suggests an interaction between cardiac myocytes and fibroblasts. In this study we examined the mechanism of cyclic mechanical stretch-induced myocytic hypertrophy, focusing on the interaction between myocytes and cardiac nonmyocytes, mostly fibroblasts. Ventricular myocytes (MCs) and cardiac nonmyocytes (NMCs) were separately extracted from neonatal rat ventricles by the discontinuous Percoll gradient method and primary cultures of cardiac cells were prepared. When MCs were co-cultured with NMCs, the size of MCs and the ANP/BNP secretion were significantly increased. This hypertrophic change of MCs in the co-culture was significantly suppressed by BQ-123, an endothelin-A (ETA) receptor antagonist. Cyclic stretch did not induce hypertrophic responses in MC culture. However, it further increased ANP/BNP production in MC-NMC co-culture (2.2-fold and 2.1-fold increases vs. non-stretch group after 48-h incubation). This increase in ANP/BNP production in the co-culture was significantly suppressed by CV-11974, an angiotensin H (Ang II) type 1 receptor antagonist. This study raises the possibility that NMCs regulate cardiocyte hypertrophy via secretion of endothelin-1 and that Ang II is involved in the interaction between MCs and NMCs during the course of hypertrophic response of cardiocytes to mechanical stretch.