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首页> 外文期刊>Life sciences >Enhanced vascular contractility in alphal-adrenergic receptor-deficient mice
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Enhanced vascular contractility in alphal-adrenergic receptor-deficient mice

机译：α1-肾上腺素能受体缺乏小鼠的血管收缩力增强

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Aim: Alphal -adrenergic receptors (alpha_1-ARs) are classified into three subtypes: alpha_1A-AR, alpha_1B-AR, and alpha_1D-AR.Triple disruption of alpha_1A-AR,alpha_1B-AR, and alpha_1D-AR genes results in hypotension and produces no contractile response of the thoracic aorta to noradrenalin. Presently, we characterized vascular contractility against other vasoconstrictors, such as potassium, prostaglandin F2alpha (PGF_2alpha) and 5-hydroxytryptamine (5-HT), in alpha_1a-AR, alpha_1B-AR, and alpha_1D-AR triple knockout (alpha_1-AR triple KO) mice.Main methods: The contractile responses to the stimulation with vasoconstrictors were studied using isolated thoracic aorta.Key findings: As a result, the phasic and tonic contraction induced by a high concentration of potassium (20 mM) was enhanced in the isolated thoracic aorta of alpha_1-AR triple KO mice compared with that of wild-type (WT) mice. In addition, vascular responses to PGF_2alpha and 5-HT were also enhanced in the isolated thoracic aorta of alpha_1-AR triple KO mice compared with WT mice. Similar to in vitro findings with isolated thoracic aorta, in vivo pressor responses to PGF_2alpha were enhanced in alpha_1-AR triple KO mice. Real-time reverse transcription-polymerase chain reaction analysis and western blot analysis indicate that gene expression of the 5-hydroxytryptamine 2A ( 5-HT_2a) receptor was up-regulated in the thoracic aorta of alpha_1-AR triple KO mice while the prostaglandin F2alpha receptor (FP) was unchanged.Significance: These results suggest that loss of alpha_1-ARs can lead to enhancement of vascular responsiveness to the vasoconstrictors and may imply that alpha_1-ARs and the subsequent signaling regulate the vascular responsiveness to other stimulations such as depolarization, 5-HT and PGF_2alpha.
机译：目的：阿尔法肾上腺素受体（alpha_1-ARs）分为三种亚型：alpha_1A-AR，alpha_1B-AR和alpha_1D-AR.alpha_1A-AR，alpha_1B-AR和alpha_1D-AR基因的三倍破坏会导致低血压和不会产生胸主动脉对去甲肾上腺素的收缩反应。目前，我们在α_1a-AR，α_1B-AR和α_1D-AR三重敲除（α_1-AR三重敲除）中表征了针对其他血管收缩剂（例如钾，前列腺素F2alpha（PGF_2alpha）和5-羟色胺（5-HT））的血管收缩能力主要方法：使用分离的胸主动脉研究了对血管收缩剂刺激的收缩反应。与野生型（WT）小鼠相比，alpha_1-AR三重KO小鼠的主动脉。另外，与WT小鼠相比，在α_1-AR三重KO小鼠的分离的胸主动脉中，对PGF_2α和5-HT的血管反应也增强了。与体外分离胸主动脉发现相似，在alpha_1-AR三重KO小鼠中，对PGF_2alpha的体内升压反应得到增强。实时逆转录-聚合酶链反应分析和免疫印迹分析表明，α_1-AR三重KO小鼠的胸主动脉中5-羟色胺2A（5-HT_2a）受体的基因表达上调，而前列腺素F2alpha受体（FP）不变。意义：这些结果表明，α_1-ARs的缺失可导致血管对血管收缩剂的反应性增强，并可能暗示α_1-ARs及其后续信号调节了血管对其他刺激（例如去极化）的反应性，5 -HT和PGF_2α。

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