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-Estradiol inhibits Angiotensin II activation of area postrema neurons
1 Department of Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA
2 Department of Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO, USA; Department of Veterinary Biomedical Sciences, University of Missouri, Columbia, MO, USA; The National Center for Gender Physiology, University of MIssouri, Columbia, MO, USA
* To whom correspondence should be addressed. E-mail: PamidimukkalaJ{at}missouri.edu.
It is well established that the area postrema, as a circumventricular organ, is susceptible to modulation by circulating hormone and peptides. Further, activation of the area postrema has been shown to modulate central neurons involved in regulation of cardiovascular function and blood pressure. In particular, the vasoactive peptide angiotensin II (Ang II) has been shown to inhibit baroreflex regulation of heart rate, increase sympathetic outflow and blood pressure via activation of the area postrema neurons. Estrogen is thought to protect against hypertension in both humans and animal models and has been shown in a number of systems to alter the effects of Ang II. The purpose of the present study was to determine the effects of estrogen on angiotensin II activation of area postrema neurons. In these studies, the effects of Ang II and KCl on Fura-2 measured cytosolic calcium ([Ca2+]i) responses in cultured area postrema neurons in the presence and absence of 12 hr exposure to 100 nM 17
-estradiol (17-E2) was evaluated. In neurons incubated in control vehicle media, 50 nM Ang II increased [Ca2+]i by 92±12%. In neurons pre-incubated with 100 nM, 17-E2, Ang II increased [Ca2+]i by only 68±11%, for a total inhibition of the Ang II evoked response of 24%. Co-application of the ER receptor antagonist ICI 182,780 did not inhibit the effects of 17-E2. In the same cells in which the effects of 17-E2 on Ang II evoked responses were tested, the effects of incubation in 17-E2 on the depolarization induced increased [Ca2+]i due to 60 mM KCl were also tested. Incubation of the cells with 100 nM 17-E2 increased the KCl evoked [Ca2+]i response and this response was blocked by ICI 182,780. These results suggest that in the area postrema, estrogen may utilize multiple pathways to modulate neural activity and responses to Ang II.
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