3 years ago

Estrogen replacement attenuates stress-induced pressor responses through vasorelaxation via β2-adrenoceptor in peripheral arteries of ovariectomized rats.

Mariko Kawahara, Akira Takamata, Sayo Omoto, Shoko Tazumi, Keiko Morimoto, Mizuho Kawakami, Naoko Yokota, Yu Nagatomo
We examined whether chronic estrogen replacement has an inhibitory effect on stress-induced pressor responses via activation of β2-adrenoceptor (AR) in peripheral arteries of ovariectomized rats. Female Wistar rats aged 9 weeks were ovariectomized. After 4 weeks, pellets containing either 17β-estradiol (E2) or placebo (Pla) were subcutaneously implanted into the rats. After 4 weeks of treatment, the rats underwent cage-switch stress and, in a separate experiment, a subset received an infusion of isoproterenol (ISO), with or without pretreatment with β1-AR blocker, atenolol or β2-AR blocker, butoxamine. In addition, isolated mesenteric artery was used to assess the concentration-related relaxing responses to ISO and the β1- or β2-AR mRNA level. The cage-switch stress-induced pressor response was significantly attenuated in the E2 group compared with the Pla group. Pretreatment with atenolol reduced the BP responses in both groups. However, butoxamine enhanced the pressor response only in the E2 group, resulting in no difference between the two groups. In addition, intravenous ISO-induced depressor response was significantly enhanced in the E2 group compared with the Pla group. Furthermore, the difference in the depressor response was abolished by pretreatment with butoxamine, but not by atenolol. In isolated mesenteric artery, butoxamine caused a rightward shift in ISO-induced concentration-related relaxation in the E2 group. The β2-AR mRNA level in mesenteric artery was higher in the E2 group than in the Pla group. These results suggest that estrogen replacement attenuated the stress-induced pressor response probably by suppressing vasoconstriction via activation of β2-AR in peripheral arteries of ovariectomized rats.

Publisher URL: http://doi.org/10.1152/ajpheart.00148.2017

DOI: 10.1152/ajpheart.00148.2017

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