Adaptive myocardial hypertrophy in the renal ablation model.
Adaptive myocardial hypertrophy in the renal ablation model.
复制标题
肾脏消融模型中的适应性心肌肥厚。
DOI：
10.1093/ajh/3.1.33
复制
发表时间：
1990
影响因子：
3.2
通讯作者：
Goodman,AI
中科院分区：
文献类型：
--
作者：
Meggs,LG;Ben-Ari,J;Gammon,D;Choudhury,M;Goodman,AI
We have previously reported downregulation of the vascular α1-receptor in the 5/6 renal ablation model. In this investigation we have examined the adaptive response of the heart following 5/6 renal ablation. Renal ablated and sham rats were maintained under identical conditions for 6 weeks. Despite the presence of systemic hypertension in renal ablated rats (185 ± 10 mm Hg,P< .01), heart weight did not differ from sham. [125I] ± CYP binding was performed and myocardial norepinephrine (NE) content determined to evaluate myocardial sympathetic neuroeffector mechanisms. Scatchard analysis and 1-isoproterenol competition curves did not reveal a difference in the binding properties of the myocardialβ-receptor. No difference in myocardial NE was found in renal ablated and sham rats. Unexpectedly, 1-isoproterenol stimulation of adenylate cyclase was impaired in renal ablated rats (32.6 ± 6v58.6 ± 5 pmol/mg/ min,P <.01) and the dose response curve shifted to the right. We conclude that despite systemic hypertension an adaptive hypertrophic response was not present in hearts of renal ablated rats; myocardial sympathetic neuroeffector mechanisms are not altered in this model; and impaired stimulation of adenylate cyclase appears to be the result of a post-receptor defect. Am J Hypertens 1990;3:33-38
