Modulation of Aortic Vascular Reactivity by Sex Hormones in a Male Rat Model of Metabolic Syndrome.
From: Department of Pathology, Instituto Nacional of Cardiología Ignacio Chávez Juan Badiano 1, Sección XVI, Tlalpan, 14080 México DF, México.
Life sciences
- Publish Date: May 2007
- ISSN: 0024-3205
- Volume: 80
- Issue: 23
- Pages: 2170-80
- Medium: Print
- Language: English
- Citation (JAMA): Torres Israel Pérez, El Hafidi Mohammed, Zamora-González José, et al. Modulation of Aortic Vascular Reactivity by Sex Hormones in a Male Rat Model of Metabolic Syndrome.. Life Sci. May 2007;80:2170-80
Abstract
Modulation by sex hormones of aortic reactivity in rats with the metabolic syndrome (MS) was investigated. The following groups of weanling male Wistar rats were used: control rats (C) received regular tap water while MS rats received 30% sucrose in their drinking water; both had rodent chow for 24 weeks. These two groups were further subdivided into the following four groups: intact (Int), castrated (Cas), castrated plus testosterone (T) and castrated plus estradiol (E). Vascular response of thoracic aortic rings to norepinephrine (NE), acetylcholine (ACh), indomethacin (Indo) and nitro-l-arginine-methyl ester (L-NAME) was investigated. Blood pressure (BP) and serum nitrates and nitrites were measured. BP and serum nitrates and nitrites were modified by castration and treatments with either T or E. Vasoconstriction in Int MS and Cas MS+T aortas was larger than in C and Cas C+T, respectively. Vasodilation in Int MS and Cas MS+T was reduced in comparison with C and Cas C+T, Cas MS and Cas MS+E. Indomethacin decreased vasoconstriction in all groups (P<0.002) but Int C and Cas C+T remained significantly smaller than Int MS and Cas MS+T. l-NAME in NE-contracted vessels induced a significant increase in vasoconstriction, except in Cas C+E rats; the responses of Int MS and Cas MS+T were significantly larger than in Int C and Cas C+T. The results suggest endothelial dysfunction in Int MS and Cas MS+T and a protective effect resulting from castration and castration plus E in MS animals, indicating a sex hormone influence.
Mesh Headings (Keywords): Animals, Aorta, Blood Pressure, Disease Models, Animal, Endothelium, Vascular, Estradiol, Gonadal Steroid Hormones, Indomethacin, Male, Metabolic Syndrome X, NG-Nitroarginine Methyl Ester, Rats, Rats, Wistar, Sucrose, Testosterone
Check for Full Text / PubMed Unique Identifier (PMID): 17499811
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