α1-Adrenoceptor subtypes in rat aorta and mesenteric small arteries are preserved during left ventricular dysfunction post-myocardial infarction
α1-Adrenoceptor subtypes in rat aorta and mesenteric small arteries are preserved during left ventricular dysfunction post-myocardial infarction
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大鼠主动脉和肠系膜小动脉中的α1-肾上腺素受体亚型在心肌梗塞后左心室功能障碍期间得以保留
DOI：
10.1016/s0008-6363(96)00261-1
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发表时间：
1997
影响因子：
10.8
通讯作者：
J. Demey
中科院分区：
文献类型：
--
作者：
F. Stassen;M. Willemsen;G. Janssen;J. Demey
目的：心力衰竭时，β-肾上腺素能受体的同源性下调导致心肌肾上腺素能反应性降低。在心肌梗死后左室功能不全的实验模型中，我们评估了稀疏神经支配和密集神经支配的外周动脉中的α1-肾上腺素受体（α1-AR）。方法：在Wistar-Kyoto大鼠（WKY）和心肌梗死（MI）或假手术（SHAM）后5周的Wistar大鼠的动脉节段中测定[3 H]哌唑嗪结合。（i）被不可逆的α1B-AR和相对选择性的α1D-AR拮抗剂氯乙可乐定（CEC）阻止;（ii）以低亲和力取代（iii）被α1A-AR选择性配体（+）-尼古地平以高亲和力（pKi 10.4）和低亲和力（pKi 7.37）置换，被α1D-AR拮抗剂BMY 7378置换。在WKY的肠系膜小动脉（MSA）中，哌唑嗪结合：（i）CEC降低50%;（ii）（+）-尼古地平以双相方式置换（pKi 8.60和pKi 6.22）;（iii）仅以低亲和力（pKi 6.86）置换BMY 7378。同样，在SHAM的TAO中，CEC阻止了哌唑嗪的结合，但30 nM（+）-尼古地平和1 nM BMY 7378都不影响它。在SHAM的MSA中，30 nM（+）-尼古地平存在时，哌唑嗪的结合几乎被消除，1 nM BMY 7378也不减少。在MI的TAO和MSA中，与SHAM相比，结合位点的密度倾向于增加而不是减少，并且对配体的亲和力和α1-AR亚型选择工具的作用均未显著改变。（2）大鼠胸主动脉中α1B-AR和α1D-AR占优势，肠系膜小动脉中α1A-AR和α1B-AR占优势;（iii）心肌梗死心力衰竭大鼠主动脉和肠系膜小动脉中α1-AR密度无明显降低。
Objective:In heart failure, homologous downregulation of β-adrenoceptors contributes to impaired adrenergic responsiveness of the myocardium. We evaluated α1,-adrenoceptors (α1-AR) in a sparsely innervated and a densely innervated peripheral artery in an experimental model of left ventricular dysfunction post-myocardial infarction.Methods:[3H]Prazosin binding was determined in arterial segments of Wistar-Kyoto rats (WKY), and of Wistar rats 5 weeks after myocardial infarction (MI) or sham operation (SHAM).Results:In the thoracic aorta (TAO) of WKY, specific prazosin binding was: (i) prevented by the irreversibleα1B-AR and relatively selective α1D-AR antagonist, chloroethylclonidine (CEC); (ii) displaced with low affinity (pKi6.25) by the α1A-AR selective ligand, (+)-niguldipine; and (iii) displaced with both high (pKi10.4) and low (pKi7.37) affinity by the α1D-AR antagonist, BMY 7378. In mesenteric small arteries (MSA) of WKY, prazosin binding was: (i) reduced 50% by CEC; (ii) displaced in a biphasic fashion by (+)-niguldipine (pKi8.60 and pKi6.22); and (iii) displaced by BMY 7378 with low affinity only (pKi6.86). Also in TAO of SHAM, prazosin binding was prevented by CEC, but neither 30 nM (+)-niguldipine nor 1 nM BMY 7378 affected it. In MSA of SHAM, prazosin binding was virtually abolished in the presence of 30 nM (+)-niguldipine and was not reduced by 1 nM BMY 7378. In TAO and MSA of MI, compared to SHAM, the density of binding sites tended to be increased rather than decreased and neither the affinity for the ligand nor the effects of α1-AR subtype selective tools were significantly modified.Conclusions:These findings indicate that: (i) radioligand binding can be applied in intact arterial segments to quantify and characterize α1-AR; (ii) although differences seem to exist between rat strains, α1B-AR and α1D-AR predominate in rat thoracic aorta and α1A-AR and α1B-AR in mesenteric small arteries; and (iii) α1-AR density is not reduced in the poorly innervated aorta and the densely innervated mesenteric small arteries of rats with heart failure due to myocardial infarction.
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新型 α-1D 肾上腺素受体对血管平滑肌收缩的具体贡献。
DOI：
--
发表时间：
1995
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Piascik,MT;Guarino,RD;Smith,MS;Soltis,EE;SaussyJr,DL;Perez,DM
通讯作者：
Perez,DM
人类正常心脏和衰竭心脏中的 Alpha-1 肾上腺素能受体。
DOI：
--
发表时间：
1988
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Bristow,MR;Minobe,W;Rasmussen,R;Hershberger,RE;Hoffman,BB
通讯作者：
Hoffman,BB
影响因子：
3.6
作者：
M. Piascik;M. S. Smith;E. E. Soltis-E.;D. Perez
通讯作者：
M. Piascik;M. S. Smith;E. E. Soltis-E.;D. Perez
患有心力衰竭的清醒犬体内β-肾上腺素能受体和内皮介导的血管舒张受到抑制。
影响因子：
20.1
作者：
Kiuchi,K;Sato,N;Shannon,RP;Vatner,DE;Morgan,K;Vatner,SF
通讯作者：
Vatner,SF
实验性心力衰竭对周围交感血管收缩的影响。
DOI：
10.1152/ajpheart.1988.254.4.h727
发表时间：
1988
期刊：
The American journal of physiology
影响因子：
--
作者：
Wilson,JR;Matthai,W;Lanoce,V;Frey,M;Ferraro,N
通讯作者：
Ferraro,N