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Giaquinto, L. R. R. Induction of kinin B1 receptor in blood vessels of angiotensin II-hypertensive rats: molecular and functional studies. 2010. 66 p. Masters thesis (Pharmacology) Instituto de Ciencias Biomedicas, Universidade de Sao Paulo, Sao Paulo, 2011. The aim of the present study was to evaluate whether angiotensin II (ANG II) infusion modulates kinin B1 receptor (B1R) mRNA and protein expression in aorta and mesenteric arterioles of the Wistar rats. It was also evaluated blood pressure, aorta and mesenteric arterioles reactivity to RB1 agonist, des-Arg9-bradykinin (DABK). Wistar rats10-weeks old were infused either with ANG II [(400ng/Kg/min) ,group ANG II] or ANG II (400ng/Kg/min) plus RB1 antagonist, des-Arg9-Leu8-bradykinin [(DAL 350ng/Kg/min) ,group ANG II + DAL] during 28 days throughout an osmotic minipump subcutaneously. As a control group, Wistar rats at the same age underwent to the same surgical procedure without the mini-pump implantation. The blood pressure was measured weekly, during 28 days, by indirect tail-cuff method.in conscious rats The B1R mRNA and protein expression were assessed by RT-PCR real-time and immunohistochemistry respectively. It was observed that ANG II infusion caused hypertension, increased RB1 mRNA expression in aorta and mesenteric arterioles when compared to the ones in the control group. The RB1 protein expression was detected in aorta, but not in mesenteric arterioles of ANG II rats. We also observed that DABK, B1R agonist, induced endothelium and nitric oxide-dependent relaxation in aortic rings isolated from ANG II rats, but not in mesenteric arterioles studied in vivo in situ and in vitro. The B1R antagonist did not interfere with the development of hypertension caused by ANG II. To evaluate the role of RB1 in the endothelial function of hypertensive rats, cumulative-concentration effect curves to acetylcholine (ACH), an endothelium-dependent vasodilator, were constructed in aortic rings isolated from ANG II, ANG II + DAL and control rats. It was observed that the maximum response (RMAX) to ACH was decreased in aortas from ANG II and ANG II + DAL rats when compared to control, characterizing endothelial dysfunction. Although the hypertension development and the endothelium dysfunction observed in the ANG II rats were not modified by DAL,the sensitivity to ACH and eNOS expression were increased. Our results allow us to conclude that ANG II modulates the expression of B1R in aorta of rats and also that B1R may contribute to some of the vascular effects of ANG II, such as endothelial dysfunction. However, this receptor did not participate in the development of hypertension caused by ANG II. Altogether, we may suggest that the ANG II and kinins interactions go further than the opposite effects classically described. In fact, they can act synergistically in the development of vascular changes in this model of arterial hypertension.

Indução de receptor B1 de cininas em vasos sanguineos de ratos hipertensos por infusão de angiotensina II: estudo molecular e funcional.