| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 1, 2003
Accepted on April 12, 2004
Graduate Center for Toxicology, Division of Pharmaceutical Sciences, Graduate Center for Nutritional Sciences, Department of Medicine, Department of Physiology
* To whom correspondence should be addressed. E-mail: lcassis{at}uky.edu.
Objective: In humans, the incidence and severity of abdominal aortic aneurysms (AAA) are greater in males than females. Chronic infusion of angiotensin II (AngII) into apolipoprotein E deficient (apoE-) mice promotes atherosclerosis and causes the formation of AAAs. Just as human males are more susceptible to developing AAAs, male mice are more susceptible to AngII-induced AAAs. We hypothesized that sex steroid hormones mediate gender differences in AngII-induced AAA through regulation of the renin angiotensin system.
Methods and Results: To define the role of ovarian hormones, female apoE- mice were subject to ovariectomy (ovx) or sham operation and infused with AngII (1,000 ng/kg/min) for 28 days. Ovx had no effect on AngII-induced atherosclerosis, nor did it influence the incidence or severity of AAA. To define the role of testicular hormones, male apoE- mice were subject to orchiectomy (orx) or sham operation and infused with AngII (1,000 ng/kg/min) for 28 days. Orx resulted in a profound reduction in AAA incidence (85% vs. 18%, sham vs. orx; P = 0.003) to a level observed in females (25%). However, orx had no effect on AngII-induced reductions in plasma renin concentration or spleen AngII receptor density. In contrast, orx resulted in an increase in atherosclerosis (0.46 ± 0.07 vs. 1.20 ± 0.21 mm2, sham vs. orx; P = 0.002).
Conclusion: These results suggest that estrogen does not mediate gender differences in AngII-induced AAA. In contrast, androgens mediate a higher incidence of AngII-induced AAA, through mechanisms that do not appear to involve circulating renin or angiotensin receptor density.
This article has been cited by other articles:
 |
|
 |
|
  T. Henriques, X. Zhang, F. B. Yiannikouris, A. Daugherty, and L. A. Cassis Androgen Increases AT1a Receptor Expression in Abdominal Aortas to Promote Angiotensin II-Induced AAAs in Apolipoprotein E-Deficient Mice Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1251 - 1256. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 H. Lu, C. M. Boustany-Kari, A. Daugherty, and L. A. Cassis Angiotensin II increases adipose angiotensinogen expression Am J Physiol Endocrinol Metab, May 1, 2007; 292(5): E1280 - E1287. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. A. Cassis, D. L. Rateri, H. Lu, and A. Daugherty Bone Marrow Transplantation Reveals That Recipient AT1a Receptors Are Required to Initiate Angiotensin II-Induced Atherosclerosis and Aneurysms Arterioscler. Thromb. Vasc. Biol., February 1, 2007; 27(2): 380 - 386. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. DAUGHERTY, D. L RATERI, and L. A CASSIS Role of the Renin-Angiotensin System in the Development of Abdominal Aortic Aneurysms in Animals and Humans Ann. N.Y. Acad. Sci., November 1, 2006; 1085(1): 82 - 91. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Daugherty, D. L. Rateri, H. Lu, T. Inagami, and L. A. Cassis Hypercholesterolemia Stimulates Angiotensin Peptide Synthesis and Contributes to Atherosclerosis Through the AT1A Receptor Circulation, December 21, 2004; 110(25): 3849 - 3857. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
