α 1d -肾上腺素受体调节α 1a -肾上腺素受体在α 1d -肾上腺素受体敲除小鼠肠系膜血管床中的血管加压作用

S. G. Martínez-Salas, J. M. Campos-Peralta, J. P. Pardo, R. Hernández-Muñoz, M. Ibarra, A. Tanoue, G. Tsujimoto, R. Villalobos-Molina
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引用次数: 3

摘要

1观察α 1a -肾上腺素能受体(α1A-AR)激动剂A61603 (N-[5-(4,5-二氢- 1h -咪唑-2-基)-2-羟基-5,6,7,8-四氢萘-1-基]甲磺酰胺)和α1-ARs激动剂苯肾上腺素在野生型(WT)小鼠和α1D-AR敲除(KO)小鼠离体肠膜血管床中的加压作用及α1-ARs拮抗剂对它们的阻断作用。2 . A61603增加WT和KO α1D-AR小鼠肠系膜血管床灌注压的表观效价分别是苯肾上腺素的86倍和138倍。3 A61603也使WT小鼠肠系膜血管床灌注压较KO α1D-AR小鼠提高约1.7倍。4 . α1A-AR选择性拮抗剂RS100329(5-甲基-3-[3-[4-[2-(2,2,2,2,-三氟乙氧基)苯基]-1-哌嗪基]丙基]-2,4-(1H)-嘧啶二酮)由于其高亲和力,在WT和KO α1A-AR小鼠肠系膜血管床中使拮抗剂浓度-反应曲线向右移动。5 α1D-AR选择性拮抗剂BMY7378(8-[2-[4-(2-甲氧基苯基)-1-哌嗪基]乙基]-8-azaspiro[4.5]癸烷-7,9-二酮)没有改变A61603或苯肾上腺素诱导的升压作用。6 α1B/ d - ar烷基化拮抗剂氯乙基氯定(CEC)使激动剂浓度-反应曲线向右偏移,并使KO α1B - ar小鼠与WT小鼠相比,苯肾上腺素诱导的最大血管收缩量减小;而CEC对A61603诱导的收缩只有轻微的改变。7结果表明,WT和KO α1D-AR小鼠离体肠系膜血管床表达α1A-AR, α1A-AR对α1D-AR的升压作用在WT小鼠中上调,提示α1B-AR在KO α1D-AR小鼠苯肾上腺素引起的血管压力中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
α1D-Adrenoceptor regulates the vasopressor action of α1A-adrenoceptor in mesenteric vascular bed of α1D-adrenoceptor knockout mice

1 The pressor action of the α1A-adrenoceptor (α1A-AR) agonist A61603 (N-[5-(4,5-dihydro-1H-imidazol-2-yl)-2-hydroxy-5,6,7,8-tetrahydronaphthalen-1-yl] methanesulfonamide) and the α1-ARs agonist phenylephrine and their blockade by selective α1-ARs antagonists in the isolated mesenteric vascular bed of wild-type (WT) mice and α1D-AR knockout (KO α1D-AR) mice were evaluated.

2 The apparent potency of A61603 to increase the perfusion pressure in the mesenteric vascular bed of WT and KO α1D-AR mice is 86 and 138 times the affinity of phenylephrine, respectively.

3 A61603 also enhanced the perfusion pressure by ≈1.7 fold in the mesenteric vascular bed of WT mice compared with KO α1D-AR mice.

4 Because of its high affinity, low concentrations of the α1A-AR selective antagonist RS100329 (5-methyl-3-[3-[4-[2-(2,2,2,-trifluoroethoxy) phenyl]-1-piperazinyl] propyl]-2,4-(1H)-pyrimidinedione) shifted the agonist concentration–response curves to the right in the mesenteric vascular bed of WT and KO α1D-AR mice.

5 The α1D-AR selective antagonist BMY7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5] decane-7,9-dione) did not modify the A61603 or the phenylephrine-induced pressor effect.

6 The α1B/D-ARs alkylating antagonist chloroethylclonidine (CEC) shifted the agonist concentration–response curves to the right and decreased the maximum phenylephrine-induced vascular contraction in KO α1D-AR mice when compared to WT mice; however, CEC only slightly modified the contraction induced by A61603.

7 The results indicate that the isolated mesenteric vascular bed of WT and KO α1D-AR mice expresses α1A-AR, that the pressor action of α1A-AR is up-regulated for α1D-AR in WT mice and suggest an important role of α1B-AR in the vascular pressure evoked by phenylephrine in KO α1D-AR mice.

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