β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats.
β3-adrenoceptors inhibit stimulated norepinephrine release in spontaneously hypertensive rats.
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DOI：
10.3389/fphys.2014.00499
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发表时间：
2014
影响因子：
4
通讯作者：
Berg T
中科院分区：
文献类型：
--
作者：
Berg T
在此，分析了β3-肾上腺素受体对血压正常和自发性高血压大鼠儿茶酚胺释放的影响。通过股动脉导管记录血压，并通过升主动脉流量记录心输出量。从流量开始到流量最大上升的时间表明正性肌力。计算总外周血管阻力（TPR）。酪胺刺激去甲肾上腺素释放，这使得突触前释放控制反映为血浆去甲肾上腺素浓度的变化。 β3-肾上腺素受体激动剂 (BRL37344) 可降低高血压大鼠的基线血管阻力、酪胺刺激的去甲肾上腺素溢出以及对酪胺的正性肌力反应，但不会降低血压正常大鼠的正性肌力反应。 β3-肾上腺素受体拮抗剂 (SR59230A) 减少两种菌株中酪胺刺激的去甲肾上腺素释放以及高血压大鼠中肾上腺素的分泌。 SR59230A 可减少血压正常大鼠中酪胺诱导的心动过速，并防止高血压大鼠中酪胺诱导的阻力升高的下调。结论是，激动剂与拮抗剂获得的矛盾结果可以通过它们与两种不同的β-肾上腺素受体的相互作用来解释：刺激去甲肾上腺素释放的BRL37344依赖性抑制和对酪胺的正性肌力反应与β3-肾上腺素受体与抑制性G蛋白偶联的刺激相一致。仅在高血压大鼠受到刺激、高水平循环儿茶酚胺期间观察到这种情况。 BRL37344 对基线血管阻力的影响与β3-肾上腺素受体与内皮一氧化氮合酶偶联的激活相一致。 SR59230A 对两种菌株中酪胺刺激的去甲肾上腺素释放的抑制作用、高血压大鼠中酪胺的 TPR 反应增加和血压正常大鼠中的心动过速可能是由于低亲和力状态 β1-肾上腺素受体（也称为推定的 β4-肾上腺素受体）的抑制所致。
Here, the influence of β3-adrenoceptors on catecholamine release in normotensive and spontaneously hypertensive rats was analyzed. Blood pressure was recorded through a femoral artery catheter, and cardiac output by ascending aorta flow. Time from onset of flow to maximum rise in flow indicated inotropy. Total peripheral vascular resistance (TPR) was calculated. Norepinephrine release was stimulated with tyramine, which allowed presynaptic release-control to be reflected as changes in the plasma norepinephrine concentration. β3-adrenoceptor agonist (BRL37344) reduced baseline vascular resistance, the tyramine-stimulated norepinephrine overflow and the positive inotropic response to tyramine in hypertensive but not normotensive rats. β3-adrenoceptor antagonist (SR59230A) reduced tyramine-stimulated norepinephrine release in both strains and the secretion of epinephrine in hypertensive rats. SR59230A reduced tyramine-induced tachycardia in normotensive rats, and prevented down-regulation of the tyramine-induced rise in resistance in hypertensive rats. It was concluded that the contradicting results obtained by agonist vs. antagonist, could be explained by their interaction with two different β-adrenoceptors: The BRL37344-dependent inhibition of stimulated norepinephrine release and positive inotropic response to tyramine was compatible with stimulation of β3-adrenoceptor coupling to inhibitory G-protein. This was observed only in hypertensive rats during stimulated, high levels of circulating catecholamines. The effect of BRL37344 on baseline vascular resistance was compatible with activation of β3-adrenoceptor coupling to endothelial nitric oxide synthase. The inhibitory effect of SR59230A on tyramine-stimulated norepinephrine release in both strains, the increased TPR-response to tyramine in hypertensive rats and tachycardia in normotensive rats may result from inhibition of the low-affinity-state β1-adrenoceptor, also known as the putative β4-adrenoceptor.
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DOI：
10.1038/oby.2004.17
发表时间：
2004-01-01
期刊：
OBESITY RESEARCH
影响因子：
--
作者：
Hao, K;Peng, SJ;Xu, XP
通讯作者：
Xu, XP
影响因子：
15.9
作者：
Gauthier, C;Tavernier, G;LeMarec, H
通讯作者：
LeMarec, H
影响因子：
7.3
作者：
Mallem, MY;Toumaniantz, G;Gauthier, C
通讯作者：
Gauthier, C
影响因子：
4.2
作者：
Cortez, Vera;Santana, Magda;Cavadas, Claudia
通讯作者：
Cavadas, Claudia
影响因子：
3.4
作者：
Berg T
通讯作者：
Berg T