DIFFERENTIAL DEVELOPMENT OF VASCULAR AND CARDIAC-HYPERTROPHY IN GENETIC-HYPERTENSION - RELATION TO SYMPATHETIC FUNCTION
DIFFERENTIAL DEVELOPMENT OF VASCULAR AND CARDIAC-HYPERTROPHY IN GENETIC-HYPERTENSION - RELATION TO SYMPATHETIC FUNCTION
复制标题
DOI：
10.1161/01.hyp.14.2.191
复制
发表时间：
1989-08-01
期刊：
影响因子：
8.3
通讯作者：
KORNER, PI
中科院分区：
文献类型：
--
作者：
ADAMS, MA;BOBIK, A;KORNER, PI
我们比较了自发性高血压大鼠（SHR）和体重匹配的血压正常的Wistar-Kyoto（WKY）大鼠在4、9、14、20、30和50周龄时的血压、后躯血管阻力特性、左心室重量和去甲肾上腺素动力学。在4周时，两种品系的收缩压和平均血压测量值相同，但SHR完全扩张后躯床的血管阻力显著高于WKY大鼠，在最大收缩期间差异更大。阻力图在最大扩张在最大收缩对体重表明，在SHR的血管肌肉质量增加的一个组成部分发生在新生儿期之前的高血压，随后由一个较晚的组件相关的血压升高。相比之下，左心室肥大在4周时最小，其发展大部分与血压升高无关。交感神经活性，评估去甲肾上腺素分数速率常数，在SHR比WKY大鼠在左心室和肾脏通过大部分的4和50周之间的时间，但在两个菌株的肌肉床相似。一旦心脏和血管肥大完全建立，这种交感神经活动模式将加重高血压。在所有地区，去甲肾上腺素组织浓度较高，在年轻的SHR，并能加强营养作用的生长因子在早期血管肥大。我们认为，初始（主要）组成部分的血管肥大之前的血压上升，可能是关键的高血压的发病机制。一旦血管“放大器”建立，年轻SHR血压升高短暂延迟的可能原因包括高血管密度、平滑肌不成熟和左心室肥大发展延迟。
We compared blood pressure, hindquarter vascular resistance properties, left ventricular weight, and norepinephrine kinetics, in spontaneously hypertensive rats (SHR) and weight-matched normotensive Wistar-Kyoto (WKY) rats at 4, 9, 14, 20, 30, and 50 weeks of age. At 4 weeks, systolic and mean blood pressure measurements were the same in both strains, but the vascular resistance of the fully dilated hindquarter bed was significantly higher in SHR than in WKY rats, with a much larger difference during maxium constriction. Plots of resistance at maximum dilation at a maxium constriction against body weight suggest that a component of the increase in vascular muscle mass in SHR occurred in the neonatal period preceding hypertension followed by a later component related to the rise in blood pressure. By contrast, left ventricular hypertrophy was minimal at 4 weeks and most of its development paralleled the rise in blood pressure. Sympathetic activity, assessed by norepinephrine fractional rate constant, was higher in SHR than in WKY rats in the left ventricular and kidney through most of the period between 4 and 50 weeks, but was similar in both strains in the muscle bed. This pattern of sympathetic activity will accentuate hypertension once cardiac and vascular hypertrophy are fully established. In all regions, norepinephrine tissue concentration was higher in young SHR and could potentiate the trophic effects of growth factors in early vascular hypertrophy. We suggest that the initial (primary) component of vascular hypertrophy precedes the rise in blood pressure and may be critical in the pathogenesis of hypertension. Possible reasons for the short delay in the rise in blood pressure in young SHR, once the vascular "amplifier" has been established, include high vascularity, immaturity of smooth muscle, and delay in the development of left ventricular hypertrophy.