Hakamata N, Hamada H, Ohsuzu F, Nakamura H
Department of Medicine I, National Defense Medical College, Tokorozawa, Saitama, Japan.
Jpn Heart J. 1997 Nov;38(6):849-57. doi: 10.1536/ihj.38.849.
Isoproterenol was continuously administered to rats at a rate of 2.5 microg/kg/min for 7 days via subcutaneously implanted osmotic minipumps. This treatment induced cardiac hypertrophy with increases in heart rate and systolic blood pressure. Beta-adrenoceptor (beta-AR) density decreased in hypertrophied hearts, but the affinity for 125I-cyanopindolol did not change. The beta-AR density decrease did not accompany the change in expression of beta1-AR mRNA. In hypertrophied hearts, adenylyl cyclase activities in the steady state, and stimulated with isoproterenol, forskolin, and manganese, decreased but there was no change in the expression of adenylyl cyclase type V mRNA. The results suggest that beta-AR downregulation and adenylyl cyclase desensitization in isoproterenol-induced cardiac hypertrophy are caused by post-transcriptional changes.
通过皮下植入渗透微型泵，以2.5微克/千克/分钟的速率连续7天给大鼠注射异丙肾上腺素。该处理导致心脏肥大，心率和收缩压升高。肥大心脏中β-肾上腺素能受体（β-AR）密度降低，但对125I-氰基吲哚洛尔的亲和力未改变。β-AR密度降低与β1-AR mRNA表达变化无关。在肥大心脏中，稳态下以及用异丙肾上腺素、福斯可林和锰刺激后的腺苷酸环化酶活性降低，但V型腺苷酸环化酶mRNA的表达没有变化。结果表明，异丙肾上腺素诱导的心脏肥大中β-AR下调和腺苷酸环化酶脱敏是由转录后变化引起的。
