【摘要】 本文通过主动脉和左肾动脉缩窄复制心功能不全大鼠模型，并采用放射配基结合实验和半定量逆转录－聚合酶链反应（ＲＴ－ＰＣＲ），从蛋白质和基因转录水平上观察在心功能不全时大鼠心脏α１－肾上腺素受体三种亚型的改变。Ｓｃａｔｃｈａｒｄ分析结果显示，在心功能不全组与对照组，大鼠心脏组织１２５Ｉ－ＢＥ与α１－肾上腺素受体结合的亲和性（２２９±３２与１９５±１５ｐｍｏｌ／Ｌ）和数量（１０２±１２与９６±１７ｆｍｏｌ／ｍｇ）均无显著差异。但ＷＢ４１０１对１２５Ｉ－ＢＥ的竞争性抑制实验显示在心功能不全组高亲和性位点所占百分比较对照组显著增高（５１±７％与２２±５％）。ＲＴ－ＰＣＲ的结果显示，在心功能不全大鼠心脏α１Ａ－ＡＲ的ｍＲＮＡ水平高于对照组，但α１Ｂ－ＡＲ的ｍＲＮＡ水平低于对照组，而α１Ｄ－ＡＲ的ｍＲＮＡ水平在两组之间没有显著差异。综合上述结果可知，在心功能不全大鼠，心脏α１Ａ－ＡＲ增加，α１Ｂ－ＡＲ下降，而α１Ｄ－ＡＲ则没有显著改变。更多还原

【Abstract】 The cardiac insufficiency was produced by simultaneous constriction of abdominalaortae and renal artery in rat. Radioligand binding and reverse transcription-polymerase chain reaction (RT-PCR) were used respectively to determine the alterations ofcardiac α1-adrenergic receptor (α1-AR) subtypes at protein level and gene transcriptionlevel. The Scatchard analysis of 125I-BE 2254 saturation curves showed that in cardiacinsufficient rat hearts the KD values (229± 32 vs 195±15 pmol/L) and the Bmax valnes (102±12 vs 96±17 fmol/mg) were not significantly different from those of control heartS. In the insufficient rat hearts, the inhibition of α1-AR specific binding byWB 4101 showed that the high affinity sites (α1A+α1D) were increased from the 22±5% of the control to 51± 7 % (P<0. 01 ). The α1A-AR mRNA level was increased,α1B--AR mRNA level decreased while α1D-AR unchanged. The results suggest that in cardiac insufficient rat hearts the subtype composition is altered as shown by increased α1A AR, decreased α1B-AR and unchanged α1D-AR, although the total amount of α1-AR isunchanged.更多还原