Alterations in sympathetic neuroeffector transmission to mesenteric arteries but not veins in DOCA-salt hypertension.

Alterations in sympathetic neuroeffector transmission to mesenteric arteries but not veins in DOCA-salt hypertension.
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DOI:
10.1016/j.autneu.2009.08.008
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发表时间:
2010-01-15
影响因子:
2.7
通讯作者:
Swain, Greg M.
Swain, Greg M.
中科院分区:
医学4区
文献类型:
--
作者:
Park, Jinwoo;Galligan, James J.;Fink, Gregory D.;Swain, Greg M.

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我们使用电流分析法监测体外去甲肾上腺素 (NE)(以氧化电流测量),研究了与高血压相关的交界前 α2 肾上腺素能受体 (α2-AR) 功能的变化。使用视频成像测量血管收缩。通过电刺激与假手术和 DOCA 盐高血压大鼠肠系膜动脉 (MA) 和静脉 (MV) 相关的交感神经来诱导 NE 释放。与假 MA 相比,DOCA 盐中的 NE 氧化电流更大;假手术和 DOCA 盐 MV 中的电流没有差异。在假 MA 中,NE 氧化电流的增加遵循多指数时间过程。在 DOCA-盐 MA 和假手术以及 DOCA-盐 MV 中,时间进程是单指数的。育亨宾(α2-AR 拮抗剂,1 μM)引起假手术和 DOCA-盐 MA 中 NE 氧化电流的单指数增加。与 DOCA-盐 MA 和 MV 相比,育亨宾在假手术中更多地增加了 NE 氧化电流和收缩。 UK 14,304(α2-AR 激动剂,1.0 μM),与假 MA 相比,DOCA-盐 MA 和假手术以及 DOCA-盐 MV 中的电流减少较少。哌唑嗪(α1-AR 拮抗剂,0.1 μM)不会改变 NE 氧化电流。与假手术 MA 相比,哌唑嗪在 DOCA 盐中更多地抑制收缩,并且几乎完全阻断假手术和 DOCA 盐 MV 中的收缩。 MA 中哌唑嗪耐药的收缩被 P2 受体拮抗剂 PPADS (10 μM) 阻断。结前 α2-AR 改变 MA 和 MV 中神经效应器连接附近的 NE 浓度。 α2-AR 功能在 MA 中最为突出,在 DOCA-盐 MA 中受损,但在 MV 中则不然。假 MA 中嘌呤能传递占主导地位。 NE 是 DOCA-盐 MA 以及假手术和 DOCA-盐 MV 中的主要血管收缩剂。
We studied hypertension-associated changes in prejunctional α2 adrenergic receptor (α2-AR) function using amperometry to monitor in vitro norepinephrine (NE) measured as oxidation currents. Vasoconstriction was measured using video imaging. NE release was induced by electrical stimulation of sympathetic nerves associated with mesenteric arteries (MA) and veins (MV) of sham and DOCA-salt hypertensive rats. NE oxidation currents were larger in DOCA-salt compared to sham MA; there were no differences between currents in sham and DOCA-salt MV. Increases in NE oxidation currents followed a multi-exponential time course in sham MA. In DOCA-salt MA and sham and DOCA-salt MV, the time course was mono-exponential. Yohimbine (α2-AR antagonist, 1 μM), caused a mono-exponential increase in NE oxidation currents in sham and DOCA-salt MA. Yohimbine increased NE oxidation currents and constrictions more in sham compared to DOCA-salt MA and compared to MV. UK 14,304 (α2-AR agonist, 1.0 μM), reduced currents less in DOCA-salt MA and sham and DOCA-salt MV compared to sham MA. Prazosin (α1-AR antagonist, 0.1 μM) did not alter NE oxidation currents. Prazosin inhibited constrictions more in DOCA-salt compared to sham MA and almost completely blocked constrictions in sham and DOCA-salt MV. Prazosin-resistant constrictions in MA were blocked by the P2 receptor antagonist, PPADS (10 μM). Prejunctional α2-ARs modify NE concentrations near neuroeffector junctions in MA and MV. α2-AR function is most prominent in MA and is impaired in DOCA-salt MA but not MV. Purinergic transmission predominates in sham MA. NE is the dominant vasoconstrictor in DOCA-salt MA and sham and DOCA-salt MV.
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