ALPHA(1)-ADRENOCEPTOR SUBTYPES MEDIATING CONTRACTION OF THE FEMORAL-ARTERY IN SPONTANEOUSLY HYPERTENSIVE RATS
ALPHA(1)-ADRENOCEPTOR SUBTYPES MEDIATING CONTRACTION OF THE FEMORAL-ARTERY IN SPONTANEOUSLY HYPERTENSIVE RATS
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DOI：
10.1139/y94-122
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发表时间：
1994-08-01
影响因子：
2.1
通讯作者：
FUJIMOTO, S
中科院分区：
文献类型：
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作者：
FUJIMOTO, S
α（1）-肾上腺素能受体（AR）根据其对布那唑嗪或哌唑嗪的不同亲和力分为α（1H）和α（1 L）亚型。α（1H）-AR进一步细分为α（1A）、α（1B）和α（1C）亚型。因此，本研究旨在确定哪些α 1-AR亚型参与了自发性高血压大鼠（SHR）中α 1-AR激动剂对股动脉制剂的激活。为了进行比较，本研究还纳入了主动脉条。在普萘洛尔、去氧皮质酮和地昔帕明的存在下，去甲肾上腺素（NE）以剂量依赖性方式收缩血管条。与Sprague-Dawley和Wistar-Kyoto大鼠（WKY）相比，SHR股动脉NE诱导收缩的负log EC（50）值和最大反应分别不变和增加。自发性高血压大鼠心脏对去甲肾上腺素的收缩反应与正常血压组织相似。α（1）-AR拮抗剂的Schild图数据表明，介导主动脉收缩的α（1）-AR亚型是同质的，对布那唑嗪（pA（2）9.4，α（1H）亚型）和WB 4101（pA（2）9.3）具有高亲和力，对5-甲基乌拉地尔（pA（2）7.7）具有低亲和力。在股动脉中，由于布那唑嗪的Schild曲线斜率小于1.0，因此存在α（1H）和α（1 L）亚型。布那唑嗪浓度为10（-9）M时，可以掩盖α（1H）亚型，布那唑嗪的Schild曲线斜率与1无差异，并降低了布那唑嗪的pA（2）值（pA（2）9.4 vs. 8.5）。氯乙可乐定抑制了主动脉和股动脉制剂对NE的反应，但没有改变5-甲基乌拉地尔的Schild图数据。结果表明，在大鼠股动脉中，α（1C）和α（1 L）亚型介导NE的收缩反应。主动脉中的α（1）-AR亚型与股动脉中的α（1H）亚型基本相同。SHR血管中介导收缩的α（1）-AR亚型与WKY组织中的相同。
alpha(1)-Adrenoceptors (ARs) were divided into alpha(1H) and alpha(1L) subtypes by their different affinities for bunazosin or prazosin. alpha(1H)-ARs were further subdivided into alpha(1A), alpha(1B), and alpha(1C) subtypes. Therefore, this study was undertaken to determine which alpha(1)-AR subtypes were involved in the activation of femoral artery preparations by alpha(1)-AR agonists in spontaneously hypertensive rats (SHR). For comparison, aortic strips were also incorporated in the present study. In the presence of propranolol, deoxycorticosterone, and desipramine, norepinephrine (NE) contracted the vascular strips in a dose-dependent manner. Negative log EC(50) values and maximum responses of NE-induced contraction of the SHR femoral artery were unchanged and increased, respectively, compared with those of Sprague-Dawley and Wistar-Kyoto rats (WKY). Contractile responses of the SHR aortae to NE were similar to those of the normotensive tissues. Schild plot data for alpha(1)-AR antagonists indicated that alpha(1)-AR subtypes mediating contraction of the aorta were homogeneous and had high affinities for bunazosin (pA(2) 9.4, alpha(1H) subtype) and WB 4101 (pA(2) 9.3) and a low affinity for 5-methylurapidil (pA(2) 7.7). In the femoral artery, because Schild plots for bunazosin had slopes of less than 1.0, there were alpha(1H) and alpha(1L) subtypes. Bunazosin, at 10(-9) M, which could mask the alpha(1H) subtype, yielded a Schild plot for bunazosin with a slope not different from unity and decreased the pA(2) value for bunazosin (pA(2) 9.4 vs. 8.5). Chlorethylclonidine inhibited the response of the aortic and femoral preparations to NE but did not change Schild plot data for 5-methylurapidil. It was suggested that in the rat femoral artery, alpha(1C) and alpha(1L) subtypes mediated the contractile response to NE. The alpha(1)-AR subtype in the aorta was essentially identical with the alpha(1H) subtype in the femoral artery. alpha(1)-AR subtypes mediating contraction in the SHR blood vessels were identical with those in the WKY tissues.