REMODELING OF THE RAT RIGHT-AND-LEFT-VENTRICLES IN EXPERIMENTAL-HYPERTENSION
REMODELING OF THE RAT RIGHT-AND-LEFT-VENTRICLES IN EXPERIMENTAL-HYPERTENSION
复制标题
DOI：
10.1161/01.res.67.6.1355
复制
发表时间：
1990-12-01
影响因子：
20.1
通讯作者：
WEBER, KT
中科院分区：
文献类型：
--
作者：
BRILLA, CG;PICK, R;WEBER, KT
肾血管性高血压的病理性左心室肥厚与细胞外间隙和心肌内冠状动脉周围的纤维胶原积聚有关。尽管血管紧张素转换酶抑制剂卡托普利以前被发现可以减轻这种间质和血管周围纤维化，但动脉和心室收缩压与循环血管紧张素II（AII）和醛固酮（AL）在促进肾血管性高血压中的肥大和胶原积累方面的相对重要性尚不确定。本研究利用左、右心室相对于冠状动脉循环的平行排列，以及心室的串联机械排列（左心室压力超负荷，右心室血压正常），试图解决这种不确定性。三个模型的实验性高血压，每一个有不同的循环AII和AL的档案，进行了检查和比较与他们的控制：肾血管性高血压，其中AII和AL增加;肾下主动脉束带，其中AII和AL是正常的;和慢性输液的AL，其中AII是抑制或正常和AL增加。在肾血管性高血压，以及与AL，我们发现了一个显着上升的间质胶原体积分数和血管周围的胶原面积的压力超载，肥厚的左心室，以及血压正常，非肥厚的右心室。尽管有相似的系统性高血压和左心室肥大，但在肾下主动脉缩窄的两个心室中均未观察到这种重构。因此，在大鼠实验性动脉高压中，心肌的肌细胞和非肌细胞隔室处于单独的控制之下：肌细胞肥大与心室负荷最密切相关，而循环AII和AL单独或与其他体液因子共同作用，调节右心室和左心室内胶原蛋白的积累。
Pathological left ventricular hypertrophy in renovascular hypertension is associated with the accumulation of fibrillar collagen within the extracellular space and around intramyocardial coronary arteries. Even though the angiotensin converting enzyme inhibitor captopril was previously found to attenuate this interstitial and perivascular fibrosis, the relative importance of arterial and ventricular systolic pressures versus circulating angiotensin II (AII) and aldosterone (AL) in promoting hypertrophy and collagen accumulation in renovascular hypertension is uncertain. By drawing on the in-parallel arrangement of the right and left ventricles, with respect to their coronary circulation, and the in-series mechanical alignment of the ventricles, with a pressure-overloaded left and a normotensive right ventricle, this study sought to address this uncertainty. Three models of experimental hypertension, each having a different circulating AII and AL profile, were examined and compared with their controls: renovascular hypertension, where both AII and AL are increased; infrarenal aorta banding, where AII and AL are normal; and a chronic infusion of AL, where AII is suppressed or normal and AL is increased. In renovascular hypertension, as well as with AL, we found a significant rise in the interstitial collagen volume fraction and perivascular collagen area of the pressure-overloaded, hypertrophied left ventricle as well as the normotensive, nonhypertrophied right ventricle. This remodeling was not seen in either ventricle with infrarenal aorta banding despite comparable systemic hypertension and left ventricular hypertrophy. Thus, in experimental arterial hypertension in the rat, myocyte and nonmyocyte compartments of the myocardium are under separate controls: myocyte hypertrophy is most closely related to ventricular loading while circulating AII and AL, acting alone or in concert with other humoral factors, regulate the accumulation of collagen within the right and left ventricles.