Androgens mediate b-adrenergic vasorelaxation impairment using adenylyl cyclase

Oscar López-Canales, Maria del Carmen Castillo-Hernández, Hilda Vargas-Robles, Amelia Rios, Jorge López-Canales, Bruno Escalante

Producción científica: Contribución a una revistaArtículorevisión exhaustiva

4 Citas (Scopus)

Resumen

Cardiovascular disease development has been associated with sex differences, suggesting that sex hormones are implicated in vascular function and development of hypertension. Vascular tone comparison at different stages of rat growth represents a good model to study testosterone-related vascular response. We explored the role of testosterone in modulation of age-dependent impaired b-adrenergic vasodilation. The 3-weekold male Sprague-Dawley rats were sorted in 3-week-old rats without any manipulation and 3-week-old rats treated with testosterone. The 9-week-old rats were randomly grouped into 9-week-old rats without any manipulation (sham), 9-week-old rats that underwent gonadectomy (9-week-old castrated), and 9- week-old castrated treated with testosterone replacement therapy (9-week-old castrated + testosterone). Vascular relaxation was evaluated in aortic rings. b-adrenergic receptor protein expression, cyclic adenosine monophosphate production, testosterone levels,and adenylyl cyclase (AC) gene expression were assessed. Testosterone levels were low in 3-week-old and 9-week-old castrated rats compared with 9-week-old sham rats. Testosterone replacement raised these levels in 3-week-old and 9-week-old castrated rats similar to those of 9-week-old sham rats. SQ22536, the AC inhibitor, prevented isoproterenol-induced relaxation in aortic rings from 3-week-old and 9-week-old castrated rats. The b-adrenergic receptor protein expression was similar in all experimental groups. AC mRNA and protein expression and cyclic adenosine monophosphate levels were elevated in 3- week-old and 9-week-old castrated rats compared with 3-weekold + testosterone, 9-week-old sham, and 9-week-old castrated + testosterone rats. In conclusion, we demonstrated that age maturation was associated with vascular relaxation impairment. Variations in testosterone levels and reduced AC expression may be responsible for this altered vascular function.

Idioma originalInglés
Páginas (desde-hasta)147-154
Número de páginas8
PublicaciónJournal of Cardiovascular Pharmacology
Volumen71
N.º3
DOI
EstadoPublicada - 1 mar. 2018
Publicado de forma externa

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