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The B2 bradykinin receptor (B2R) is a G protein-coupled receptor (GPCR) that is constitutively expressed in various tissues, including vascular endothelium and smooth muscle [1, 6]. In rabbits, as in humans, it serves as the primary mediator for the physiological actions of bradykinin, a potent vasodilator and inflammatory mediator [2, 3]. Activation of the B2R leads to increased vascular permeability, vasodilation, and pain, primarily through Gq-mediated signaling and calcium mobilization [1, 10]. It plays a critical role in the pathophysiology of hereditary angioedema (HAE), where excessive bradykinin production leads to life-threatening swelling [1, 8]. Therapeutic strategies often focus on B2R antagonism to treat acute HAE attacks and other inflammatory conditions [4, 5]. Rabbit models are frequently used in pharmacological studies because the rabbit B2R shows high sequence homology and similar pharmacological profiles to the human receptor [3, 10].
Antagonism of the B2 bradykinin receptor to inhibit the pro-inflammatory and vasodilatory effects of bradykinin.
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