The aim of this study was to assess the influence of the endogenous status of ovarian hormones on the relaxation induced by the beta-adrenoceptor agonists isoprenaline (isoproterenol) and dobutamine in thoracic aorta segments, precontracted with noradrenaline, from age-matched (13-week-old) virgin (oestrus) and ovariectomized (OVX) prepubertal female Wistar rats. Isoprenaline-induced relaxation was decreased in intact aortic segments from OVX rats compared with that in segments from oestrus rats. Relaxation was significantly reduced by endothelium removal, 1 micromol/l propranolol or 100 micromol/l N(G)-nitro-L-arginine methyl ester (L-NAME). The beta(1)-adrenoceptor agonist dobutamine induced less relaxation in intact arteries from oestrus rats than did isoprenaline, and dobutamine-induced relaxation was markedly less in intact segments from OVX compared with oestrus rats. This dobutamine-induced relaxation was abolished by endothelium removal, and reduced by 1 micromol/l propranolol, 100 micromol/l L-NAME or 1 micromol/l yohimbine. Cholera toxin (an activator of the stimulatory G-protein G(s)) caused relaxation in intact arteries from oestrus rats; this relaxation was decreased by both deprivation of ovarian hormones and endothelium removal. Forskolin (a direct activator of the catalytic subunit of adenylate cyclase) and sodium nitroprusside (a nitric oxide donor and cGMP-dependent vasodilator agonist) induced similar endothelium-independent relaxation in arteries from both oestrus and OVX rats. These results suggest that the relaxation elicited by endothelial beta-adrenoceptor activation in the rat thoracic aorta is impaired by deprivation of female ovarian hormones; this impairment is caused, at least in part, by decreases in both the endothelial release of NO and G(s) function.

译文

这项研究的目的是评估卵巢激素的内源性状态对 β-肾上腺素受体激动剂异丙肾上腺素 (异丙肾上腺素) 和多巴酚丁胺在胸主动脉段中诱导的松弛的影响,来自年龄匹配的 (13周大) 处女 (发情期) 和去卵巢 (OVX) 青春期前雌性Wistar大鼠。与发情大鼠相比,OVX大鼠完整主动脉段异丙肾上腺素诱导的松弛减少。通过内皮去除,1微mol/l普萘洛尔或100微mol/l N(G)-硝基-L-精氨酸甲酯 (l-name) 显着降低松弛。与异丙肾上腺素相比,β (1)-肾上腺素受体激动剂多巴酚丁胺在发情期大鼠的完整动脉中引起的松弛较少,而多巴酚丁胺在OVX的完整节段中引起的松弛明显较少。这种多巴酚丁胺诱导的松弛通过内皮去除消除,并被1微摩尔/升普萘洛尔、100微摩尔/升l-name或1微摩尔/升育亨宾还原。霍乱毒素 (刺激性g蛋白G(s) 的激活剂) 引起发情大鼠完整动脉的松弛; 卵巢激素的剥夺和内皮的去除均降低了这种松弛。Forskolin (腺苷酸环化酶催化亚基的直接激活剂) 和硝普钠 (一氧化氮供体和cGMP依赖性血管扩张激动剂) 在发情和OVX大鼠的动脉中诱导了类似的非内皮依赖性舒张。这些结果表明,剥夺女性卵巢激素会损害大鼠胸主动脉中内皮 β-肾上腺素受体激活引起的松弛; 这种损害至少部分是由NO和G(s) 功能的内皮释放减少引起的。

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