Visceral periadventitial adipose tissue regulates arterial tone of mesenteric arteries
Visceral periadventitial adipose tissue regulates arterial tone of mesenteric arteries
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DOI：
10.1161/01.hyp.0000140058.28994.ec
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发表时间：
2004-09-01
期刊：
影响因子：
8.3
通讯作者：
Gollasch, M
中科院分区：
文献类型：
--
作者：
Verlohren, S;Dubrovska, G;Gollasch, M
外膜周围脂肪组织产生影响血管收缩的血管活性物质。早期的研究在主动脉中解决了这个问题，主动脉是一种不会导致外周血管阻力的血管。我们检验了外膜周围脂肪组织调节与血压调节更相关的小动脉收缩的假设。我们研究了成年雄性Sprague-Dawley大鼠肠系膜动脉环外膜周围脂肪组织。与无外膜周脂肪的血管相比，完整血管对5-羟色胺、苯肾上腺素和内皮素I的收缩反应明显降低。对U46619或去极化高K+溶液（60 mmol/L）的收缩反应在有和无外膜周围脂肪的血管中相似。K+通道开放剂cromakalim诱导5-羟色胺预收缩的血管舒张，但不诱导U46619或高K+溶液（60 mmol/L）预收缩的血管舒张，表明K+通道参与其中。完整血管平滑肌细胞的细胞内膜电位比无外膜脂肪的血管更超极化。用4-氨基吡啶（2 mmol/L）或3，4-二氨基吡啶（1 mmol/L）抑制延迟整流钾通道（K-v），可消除其抗收缩作用和外膜脂肪膜超极化。用格列本脲（3 mumol/L）、蜂毒肽（1 mumol/L）、伊比利亚毒素（100 nmol/L）、四乙基铵离子（1 mmol/L）、四戊基铵离子（10 mumol/L）或Ba 2+（3 mumol/L）阻断其他K+通道无影响。纵向去除一半的血管周围组织，减少了近50%的脂肪的抗收缩作用，而去除内皮细胞没有影响。我们认为内脏外膜周围脂肪组织通过激活血管平滑肌细胞的K-v通道诱导血管舒张来控制肠系膜动脉张力。
Periadventitial adipose tissue produces vasoactive substances that influence vascular contraction. Earlier studies addressed this issue in aorta, a vessel that does not contribute to peripheral vascular resistance. We tested the hypothesis that periadventitial adipose tissue modulates contraction of smaller arteries more relevant to blood pressure regulation. We studied mesenteric artery rings surrounded by periadventitial adipose tissue from adult male Sprague-Dawley rats. The contractile response to serotonin, phenylephrine, and endothelin I was markedly reduced in intact vessels compared with vessels without periadventitial fat. The contractile response to U46619 or depolarizing high K+-containing solutions ( 60 mmol/L) was similar in vessels with and without periadventitial fat. The K+ channel opener cromakalim induced relaxation of vessels precontracted by serotonin but not by U46619 or high K+-containing solutions ( 60 mmol/L), suggesting that K+ channels are involved. The intracellular membrane potential of smooth muscle cells was more hyperpolarized in intact vessels than in vessels without periadventitial fat. Both the anticontractile effect and membrane hyperpolarization of periadventitial fat were abolished by inhibition of delayed-rectifier K+ (K-v) channels with 4-aminopyridine ( 2 mmol/L) or 3,4-diaminopyridine ( 1 mmol/L). Blocking other K+ channels with glibenclamide ( 3 mumol/L), apamin ( 1 mumol/L), iberiotoxin ( 100 nmol/L), tetraethylammonium ions ( 1 mmol/L), tetrapentylammonium ions ( 10 mumol/L), or Ba2+ ( 3 mumol/L) had no effect. Longitudinal removal of half the perivascular tissue reduced the anticontractile effect of fat by almost 50%, whereas removal of the endothelium had no effect. We suggest that visceral periadventitial adipose tissue controls mesenteric arterial tone by inducing vasorelaxation via K-v channel activation in vascular smooth muscle cells.