The beneficial vascular effects of ralixofene could, in part, be explained by its partial agonist profile towards the BK B2 receptor [36]. Thus, in a study aimed at assessing the vasoprotective effects of the compound, rats treated with raloxifene showed an increased reduction of systolic blood pressure on administration of bradykinin, suggesting an enhanced bioavailability of NO in these animals [37]. Moreover, diverse experiments subsequently confirmed a role of raloxifene inducing endothelium-dependent relaxation as due to the upregulation of nitric-oxide synthase (eNOS) expression [38,39,40]. Although these results can be due to the partial agonist profile of raloxifene reported in this work [33], the effect can also be explained as due to the activation of the GPR30 receptor [41]. Accordingly, further experimental work is necessary to differentiate both effects.