Cardiovascular Adrenoreceptor Number and Function in Experimental Hypertension in the Baboon
Cardiovascular Adrenoreceptor Number and Function in Experimental Hypertension in the Baboon
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狒狒实验性高血压中心血管肾上腺素受体的数量和功能
DOI：
10.1097/00005344-198500076-00030
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发表时间：
1985
影响因子：
3
通讯作者：
C. Rosendorff
中科院分区：
文献类型：
--
作者：
M. Hurwitz;C. Rosendorff
我们使用氚化哌唑嗪（α1-拮抗剂）研究了狒狒高血压模型（Grollman 2-肾，2 -8字形）心肌和合并动脉平滑肌膜中肾上腺素受体密度和亲和力。育亨宾（α2-拮抗剂）和二氢烯丙洛尔β-拮抗剂）作为配体。到24周结束时，平均动脉血压从105 ± 3 mmHg升高至155 ± 8 mmHg。心率由102 ± 6次/min增加到118 ± 2次/min。心肌α2和β受体密度显著降低，α2、α2和β受体KD值显著降低。在动脉膜中。α1-和α2-受体的Bmax增加了一倍以上，两种受体亚型的Kd值均显著增加。心肌β-受体密度的降低可能代表了对这种类型高血压中交感神经活动增加的下调反应，心肌α2-受体的Bmax降低可能导致交感神经末梢释放去甲肾上腺素的反馈抑制降低，从而导致心率增加。动脉中两种α受体亚型的增加可能是高血压发病机制的一部分。然而，我们无法显示对输注异丙肾上腺素的变时性反应增加，或对苯肾上腺素的血压反应增加。
We studied adrenoreceptor density and affinity in the myoeardial and pooled arterial smooth muscle membranes in a baboon model (Grollman 2-kidney, 2-figure-of-8) of hypertension, using tritiated prazosin (α1-antagonist). yohimbine (α2-antagonist) and dihydroalprenolol β-antagonist) as ligands. By the end of 24 weeks, mean arterial blood pressure had increased from 105 ± 3 to 155 ± 8 mm Hg. and heart rate increased from 102 ± 6 to 118 ± 2/min. In the myocardium, there was a significant decrease in α2- and β-receptor density, and significant decreases in α2-, α2- and β-receptor KD values. In membranes from arteries. Bmax for α1- and α2-receptors more than doubled, with significantly increased Kd values for both receptor subtypes. The decrease in myocardial β-receptor density may represent a down-regulatory response to the increased sympathetic activity in this type of hypertension, and the decreased Bmax for myocardial α2-receptors may cause a decreased feedback inhibition of norepinephrine release from sympathetic nerve terminals, contributing to the increased heart rate. The increase in both α-receptor subtypes in arteries may be part of the pathogenesis of the hypertension. However we were unable to show increased chronotropic responses to infused isoproterenol, or increased blood pressure responses to phenylephrine.