期刊
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
卷 28, 期 7, 页码 1251-1256出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/ATVBAHA.107.160382
关键词
angiotensin; aneurysms; androgen; atherosclerosis; sex hormones
资金
- NHLBI NIH HHS [P01 HL080100, P01 HL080100-030001, P01 HL080100-040001, P01 HL080100-020001, P01 HL080100-01A10001] Funding Source: Medline
Objective-Castration of male apolipoprotein E-deficient (apoE(-/-)) mice reduces angiotensin II (AngII)-induced abdominal aorta aneurysms (AAAs) to that of female mice. The purpose of this study was to determine whether this reduction is attributable to androgen-mediated regulation of aortic Ang II type 1A receptors (AT1aR). Methods and Results-AT1aR mRNA abundance in the AAA-prone region of abdominal aortas was 8-fold greater compared to thoracic aortas of male but not female mice. AT1aR mRNA abundance decreased after castration in abdominal but not thoracic aortas of male mice. Dihydrotestosterone (DHT, 0.16 mg/d) administration to castrated male mice restored AT1aR mRNA abundance in abdominal aortas but had no effect in thoracic aortas. DHT also increased AT1aR mRNA abundance in abdominal aortas from female mice. Castrated male or female apoE(-/-) mice were administered DHT during infusion of saline or Ang II (1000 ng/kg/min for 28 days). DHT administration did not alter serum cholesterol concentrations, lipoprotein distributions, or atherosclerotic lesion areas in either male or female mice. However, administration of DHT increased AAA incidence in male (27% placebo versus 75% DHT) and female mice (28% placebo versus 64% DHT). Conclusions-Androgen promotes AT1aR mRNA abundance in abdominal aortas associated with increased Ang II-induced AAAs.
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