Altered β1-3-adrenoceptor influence on α2-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats.
Altered β1-3-adrenoceptor influence on α2-adrenoceptor-mediated control of catecholamine release and vascular tension in hypertensive rats.
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DOI：
10.3389/fphys.2015.00120
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发表时间：
2015
影响因子：
4
通讯作者：
Berg T
中科院分区：
文献类型：
--
作者：
Berg T
α - 2和β-肾上腺素受体（AR）相互控制儿茶酚胺的释放和血管张力。这些功能紊乱存在于自发性高血压大鼠（SHR）中。本研究测试α2AR功能障碍是否由α2AR/βAR相互作用改变引起。通过股动脉导管记录血压，通过升主动脉血流探头记录心输出量。计算外周血管总阻力（TPR）。15分钟的酪胺输注刺激去甲肾上腺素释放，这使得突触前释放控制反映为向血浆溢出的差异。手术应激刺激肾上腺素分泌。L-659,066 （α 2ar拮抗剂）增强了正常血压对照组（WKY）的去甲肾上腺素溢出，但对SHR没有作用。纳多洛尔（β1+2）和ICI-118551 (β2)，但阿替洛尔（β1）和SR59230A [β(3)/1L]没有阻止这种增加。所有βAR拮抗剂允许L-659,066增加酪胺诱导的SHR中去甲肾上腺素溢出和两种菌株的肾上腺素分泌。米利酮和β3AR激动剂（BRL37344）抑制camp降解，增强了L-659,066对SHR中儿茶酚胺和WKY中肾上腺素释放的影响。β1/2AR拮抗剂和BRL37344在WKY中反对l -659,066依赖性消除tpr对酪胺的反应。α2AR/βAR拮抗剂对SHR的tpr反应影响不大。米立酮增强了酪胺对tpr反应的l -659,066依赖性降低。结论：β2AR活性是α2AR自抑制WKY去甲肾上腺素释放的必要底物。β1+2AR拮抗α2AR抑制SHR中去甲肾上腺素的释放和两种菌株的肾上腺素分泌。SHR中不存在βAR-α2AR对血管张力的相互控制。选择性激动剂激活β3AR-Gi信号，影响酪胺诱导的WKY tpr反应和SHR儿茶酚胺释放。
α2- and β-adrenoceptors (AR) reciprocally control catecholamine release and vascular tension. Disorders in these functions are present in spontaneously hypertensive rats (SHR). The present study tested if α2AR dysfunctions resulted from altered α2AR/βAR interaction. Blood pressure (BP) was recorded through a femoral artery catheter and cardiac output by an ascending aorta flow probe. Total peripheral vascular resistance (TPR) was calculated. Norepinephrine release was stimulated by a 15-min tyramine-infusion, which allows presynaptic release-control to be reflected as differences in overflow to plasma. Surgical stress activated some secretion of epinephrine. L-659,066 (α2AR-antagonist) enhanced norepinephrine overflow in normotensive controls (WKY) but not SHR. Nadolol (β1+2) and ICI-118551 (β2), but not atenolol (β1) or SR59230A [β(3)/1L] prevented this increase. All βAR antagonists allowed L-659,066 to augment tyramine-induced norepinephrine overflow in SHR and epinephrine secretion in both strains. Inhibition of cAMP-degradation with milrinone and β3AR agonist (BRL37344) enhanced the effect of L-659,066 on release of both catecholamines in SHR and epinephrine in WKY. β1/2AR antagonists and BRL37344 opposed the L-659,066-dependent elimination of the TPR-response to tyramine in WKY. α2AR/βAR antagonists had little influence on the TPR-response in SHR. Milrinone potentiated the L-659,066-dependent reduction of the TPR-response to tyramine. Conclusions: β2AR activity was a required substrate for α2AR auto inhibition of norepinephrine release in WKY. β1+2AR opposed α2AR inhibition of norepinephrine release in SHR and epinephrine secretion in both strains. βAR-α2AR reciprocal control of vascular tension was absent in SHR. Selective agonist provoked β3AR-Gi signaling and influenced the tyramine-induced TPR-response in WKY and catecholamine release in SHR.
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影响因子：
3.4
作者：
Berg T;Jensen J
通讯作者：
Jensen J
影响因子：
4
作者：
Berg T
通讯作者：
Berg T
影响因子：
5
作者：
Berg, T
通讯作者：
Berg, T
影响因子：
7.3
作者：
Mallem, MY;Toumaniantz, G;Gauthier, C
通讯作者：
Gauthier, C
影响因子：
5.5
作者：
Queen, Lindsay R.;Ji, Yong;Ferro, Albert
通讯作者：
Ferro, Albert