4.5 Article

Hydrogen sulfide derived from periadventitial adipose tissue is a vasodilator

期刊

JOURNAL OF HYPERTENSION
卷 27, 期 11, 页码 2174-U3

出版社

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/HJH.0b013e328330a900

关键词

adipocyte-derived relaxing factor; cystathionine gamma-lyase; hydrogen sulfide; hypertension; periadventitial adipose tissue

资金

  1. Major State Basic Research Development Program of the People's Republic of China [2006CB503807]
  2. National Basic Research Program of China [2009CB941603]
  3. National Natural Science Foundation of the People's Republic China [30400151, 30572072]

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Background Recently, periadventitial adipose tissue (PAT) was found to secrete bioactive factors playing an important role in the regulation of vascular tension. Hydrogen sulfide (H2S), a novel cardiovascular gasotransmitter, relaxes vessels through the K-ATP channel in a calcium-dependent and endothelial-independent manner. Methods We first identified the endogenous H2S-generated key enzyme cystathionase (CSE) expressed in adipocytes of PAT and H2S released from PAT in rats. Results The CSE inhibitors DL-propargylglycine and/or beta-cyano-L-alanine largely blocked the vasorelaxing effects on aorta rings (removed adventitia), induced by PAT, the culture medium of PAT or isolated adipocytes from PAT. Phenylephrine, serotonin and angiotensin II inhibited endogenous H2S production from the aortic medium but increased its release from PAT. Endogenous H2S generated in the aorta and PAT was decreased but the level of CSE protein was increased with the aging of rats. In rats with hypertension induced by abdominal aortic banding, H2S generation and CSE protein expression were significantly increased in PAT but not aortic tissues. Transplanting PAT into periadventitia of stenotic aortas ameliorated the elevated arterial blood pressure and decreased angiotensin II level in aorta. Conclusion These results suggested PAT could endogenously generate H2S, which might act as an adipocyte-derived relaxing factor and contribute to the pathogenesis of hypertension. J Hypertens 27: 2174-2185 (C) 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins.

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