The endothelin receptor antagonist, BQ-123, inhibits angiotensin II-induced contractions in rabbit aorta
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2014, Clinical TherapeuticsCitation Excerpt :Along this line, Thaete et al61 recently reported that a small-molecule inhibitor of the ETA receptor antagonist ABT-546 was maternally restricted, with fetal exposure at only ~2% of maternal levels. Likewise, a number of small-peptide–based inhibitors of the ETA receptor have been described which, if stabilized for better pharmacologic parameters and fetal exclusion, could be a potent approach to managing the maternal symptoms of preeclampsia.62 Preeclampsia remains an enigmatic disorder of pregnancy, with an incomplete understanding of its etiology and a lack of therapeutic options for the clinical practitioner.
Endothelium-derived vasoactive agents, AT1 receptors and inflammation
2011, Pharmacology and TherapeuticsCitation Excerpt :In addition, ET-1 treatment of isolated EC stimulates the conversion of Ang I to Ang II via enhancing local ACE activity (Kawaguchi et al., 1991) suggesting that ET-1 and Ang II peptides may have the capacity to increase the quantity of each other. In isolated rabbit aorta ET-1 receptor antagonism resulted in reduction in the vasoconstrictor response to Ang II (Webb et al., 1992). Moreover, in vivo, infusion of Ang II was also shown to enhance levels of ET-1 in the rat in a way that was blocked by ET-1 receptor (Moreau et al., 1997) and AT1R antagonism (d'Uscio et al., 1998), whilst blockade of ET-1 receptors was shown to prevent the hemodynamic changes induced by low (but not high) doses of Ang II (Balakrishnan et al., 1996).
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