Hyperinsulinemia blunts sympathetic vasoconstriction: a possible role of β-adrenergic activation.
Hyperinsulinemia blunts sympathetic vasoconstriction: a possible role of β-adrenergic activation.
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高胰岛素血症减弱交感血管收缩：β-肾上腺素能激活的可能作用。
DOI：
10.1152/ajpregu.00018.2021
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发表时间：
2021
期刊：
影响因子：
--
通讯作者：
Padilla,Jaume
中科院分区：
文献类型：
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作者：
Limberg,JacquelineK;Soares,RogerioN;Power,Gavin;Harper,JenniferL;Smith,JamesA;Shariffi,Brian;Jacob,DainW;Manrique-Acevedo,Camila;Padilla,Jaume
在此，我们报告了健康年轻男性（n= 14）和女性（n= 12）的样本，高胰岛素血症诱导总外周抵抗的时间依赖性降低及其对维持血压的贡献。在同样的参与者中，我们观察到胰岛素在下肢的血管扩张作用，尽管伴随的是交感神经系统的激活。我们假设这种明显的外周血管舒张可能是由于腿部血管在全身胰岛素刺激时逃避交感血管收缩的能力。与这一观点一致，我们在健康男性（n= 9）和女性（n= 7）的一个亚组中证明，全身输注胰岛素会减弱由冷压试验引起的交感神经介导的腿部血管收缩，冷压试验是一种公认的交感神经兴奋性刺激。进一步证实了这一观察，我们在小鼠主动脉环中发现胰岛素暴露抑制肾上腺素和去甲肾上腺素诱导的血管收缩。值得注意的是，我们发现这种胰岛素对儿茶酚胺诱导的收缩的抑制作用在β-肾上腺素能受体阻断后减弱。与此同时，我们也发现胰岛素增强了β-肾上腺素能介导的血管舒张。总的来说，这些发现支持这样一种观点，即男性和女性腿部血管在全身性高胰岛素血症期间交感血管收缩可以减弱，这种现象可能部分是由β-肾上腺素能血管舒张的增强中和α-肾上腺素能血管收缩介导的。
Herein we report in a sample of healthy young men (n= 14) and women (n= 12) that hyperinsulinemia induces time-dependent decreases in total peripheral resistance and its contribution to the maintenance of blood pressure. In the same participants, we observe profound vasodilatory effects of insulin in the lower limb despite concomitant activation of the sympathetic nervous system. We hypothesized that this prominent peripheral vasodilation is possibly due to the ability of the leg vasculature to escape sympathetic vasoconstriction during systemic insulin stimulation. Consistent with this notion, we demonstrate in a subset of healthy men (n= 9) and women (n= 7) that systemic infusion of insulin blunts sympathetically mediated leg vasoconstriction evoked by a cold pressor test, a well-established sympathoexcitatory stimulus. Further substantiating this observation, we show in mouse aortic rings that insulin exposure suppresses epinephrine and norepinephrine-induced vasoconstriction. Notably, we found that such insulin-suppressing effects on catecholamine-induced constriction are diminished following β-adrenergic receptor blockade. In accordance, we also reveal that insulin augments β-adrenergic-mediated vasorelaxation in isolated arteries. Collectively, these findings support the idea that sympathetic vasoconstriction can be attenuated during systemic hyperinsulinemia in the leg vasculature of both men and women and that this phenomenon may be in part mediated by potentiation of β-adrenergic vasodilation neutralizing α-adrenergic vasoconstriction.