Muders F, Kromer E P, Bahner U, Elsner D, Ackermann B, Schunkert H, Palkovits M, Riegger G A
Klinik und Poliklinik für Innere Medizin II, University of Regensberg, Germany.
Cardiovasc Res. 1995 Mar;29(3):416-21.
In several forms of heart disease characterised by low cardiac output, activated neurohumoral systems including increased vasopressin plasma levels play a key role in the changes in cardiovascular function. The aim of this study was to test the hypothesis that under such conditions the central vasopressin system might also be altered, which could contribute to deranged cardiovascular control.
Aortic stenosis was produced in 22 rats by placing a Silver clip (inner diameter 0.6 mm) on the ascending aorta. After 12 weeks, haemodynamic and hormonal measurements were performed, and vasopressin content was determined in 20 microdissected brain areas (micropunch technique). Twenty two sham operated rats served as controls.
Twelve weeks after placing the supravalvular clip, significant aortic stenosis was documented by left ventricular myocardial hypertrophy. Cardiac index was significantly reduced and the peripheral vascular resistance index was increased, while poststenotic aortic pressure was non-significantly decreased. Plasma renin concentration [6.8(SEM 0.9) v 2.1(0.2) ngAI.ml-1.h-1 in controls] and plasma vasopressin [32.9(12.5) v 18.4(6.0) pg.ml-1] were significantly increased, while plasma and urinary noradrenaline remained unaltered. The vasopressin content was significantly altered in eight out of 20 brain areas investigated. Concerning the vasopressin producing hypothalamic nuclei, concentrations were increased in the paraventricular [7494(360) v 4744(237) pg.mg-1 protein, P < 0.05] and suprachiasmatic [3613(170) v 1784(197) pg.mg-1 protein, P < 0.01], but not in the supraoptic nuclei. Rats with aortic stenosis showed significantly raised vasopressin concentrations in the median eminence [25 186(1682) v 37 367(1345) pg.mg-1 protein, P < 0.01], where the hormone is mainly concentrated in the hypothalamo-hypophysial tract. Vasopressin content was significantly decreased in locus coeruleus [49(5) v 89(6) pg.mg-1 protein], which is known to be involved in modulation of sympathetic activity.
As well as showing increased secretion of vasopressin into the blood with consecutive peripheral antidiuretic and vasoconstrictive effects, these data suggest an alteration in the central vasopressin system in aortic stenosis which might transmit cardiovascular effects by neuromodulation and neuroregulation.
在几种以心输出量降低为特征的心脏病中，包括血管加压素血浆水平升高在内的激活的神经体液系统在心血管功能变化中起关键作用。本研究的目的是检验这样一种假设，即在这种情况下，中枢血管加压素系统也可能发生改变，这可能导致心血管控制紊乱。
通过在22只大鼠的升主动脉上放置一个银夹（内径0.6毫米）来制造主动脉狭窄。12周后，进行血流动力学和激素测量，并通过微量解剖技术测定20个脑区的血管加压素含量。22只假手术大鼠作为对照。
在放置瓣膜上夹12周后，左心室心肌肥厚证明存在明显的主动脉狭窄。心脏指数显著降低，外周血管阻力指数升高，而狭窄后主动脉压无显著降低。血浆肾素浓度[对照组为6.8（标准误0.9）对2.1（0.2）纳克AI·毫升-1·小时-1]和血浆血管加压素[32.9（12.5）对18.4（6.0）皮克·毫升-1]显著升高，而血浆和尿去甲肾上腺素保持不变。在所研究的20个脑区中，有8个脑区的血管加压素含量发生了显著改变。关于产生血管加压素的下丘脑核，室旁核[7494（360）对4744（237）皮克·毫克-1蛋白质，P<0.05]和视交叉上核[3613（170）对1784（197）皮克·毫克-1蛋白质，P<0.01]中的浓度升高，但视上核中未升高。主动脉狭窄大鼠的正中隆起中血管加压素浓度显著升高[25186（1682）对37367（1345）皮克·毫克-1蛋白质，P<0.01]，该激素主要集中在下丘脑-垂体束中。蓝斑中的血管加压素含量显著降低[49（5）对89（6）皮克·毫克-1蛋白质]，已知蓝斑参与交感神经活动的调节。
这些数据表明，除了血管加压素向血液中的分泌增加并伴有连续的外周抗利尿和血管收缩作用外，主动脉狭窄时中枢血管加压素系统也发生了改变，这可能通过神经调节和神经调控传递心血管效应。
