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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：在α-肾上腺素能受体缺陷小鼠中增强血管收缩性

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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：α-肾上腺素能受体（α_1-ARS）分为三种亚型：α_1a-ar，α_1b-ar和alpha_1d-ar.tha -1a-Ar，α_1b-ar和α_1d-ar基因的α_1d-ar和α_1d-ar基因导致低血压和没有胸部主动脉的收缩响应到诺肾上腺素。目前，我们在α_1A-AR，Alpha_1B-AR和Alpha_1D-AR三重敲除（Alpha_1-AR三重KO ）MICE.MAIN方法：使用孤立的胸主动脉进行血管收缩仪对刺激的收缩反应。结果，在分离的胸部中，通过高浓度的钾（20mM）诱导的序号和补品收缩Alpha_1-Ar三重KO小鼠的主动脉与野生型（WT）小鼠相比。此外，与WT小鼠相比，在α_1-AR三重KO小鼠的分离的胸主动脉中还增强了对PGF_2Alpha和5-HT的血管反应。与孤立的胸主动脉的体外发现类似，在体内压力响应中，在α_1-AR三重KO小鼠中增强了对PGF_2Alpha的反应。实时逆转录 - 聚合酶链反应分析和蛋白质印迹分析表明，在前列腺素F2Alpha受体的同时，在α_1-AR三重KO小鼠的胸主动脉中上调5-羟基对胺2a（5-ht_2a）受体的基因表达（FP）没有改变。重要性：这些结果表明，α1-ars的丧失可以导致对血管收缩仪的血管反应性提高，并且可能意味着α_1-ars和随后的信号传导调节对其他刺激的血管反应，例如去极化，5 -ht和pgf_2alpha。

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