The kalikrein–kinin system plays an important role in the mainten

The kalikrein–kinin system plays an important role in the maintenance of cardiovascular homeostasis. In this regard, the kinin B2R null mice

present high sensitivity to hypertensive stimuli [1] and [5], impairment of endothelium-dependent vasodilation and decrease in NO bioavailability [15]. Moreover, studies have indicated the existence of functional interactions between angiotensin and kinin receptors in vascular cells. In this respect, Seyed et al. [29] demonstrated that Ang II-mediated vasodilation in coronary vessels from dogs is dependent of B2R. find more This interaction was also observed in arteries from normotensive [9] and [19] and hypertensive rats [21]. The present data suggest that Ang II-induced constriction is also counterbalanced by B2R activation in venules and veins from hypertensive rats. Therefore, the final effects resulted from Ang II, at least on these vascular beds, should be considered as a combination of AT1R signaling in the presence of a modulating action elicited by B2R. Further studies will reveal the physiological and OSI-744 manufacturer pathophysiological consequences of this phenomenon. Whereas COX metabolites appear to counterbalance the Ang II-induced venoconstriction in

SHR, our data do not suggest the participation of NO in this effect. In normotensive rats, Fernandes et al. [8] demonstrated that NO counteracts the Ang II-induced venoconstriction, while COX metabolites were not involved in this response. Similar results were observed in mesenteric arterioles from normotensive rats [19]. It has been suggested that alteration in NO metabolism is implicated in endothelial dysfunction, a common denominator in essential hypertension [7]. In fact, several vascular beds of SHR present impaired endothelium-dependent vasodilation [14], [17] and [33]. In this regard, increased production of superoxide anion in vessels of SHR has been associated to NO inactivation and elevation of the blood pressure [28]. Our data suggest that production of vasodilatory eicosanoids

in venous bed from SHR represent an alternative pathway to attenuate the Ang II-induced constriction at low levels of NO. Moreover, COX metabolites probably are involved in impairment of Ang II-induced constriction Astemizole in portal vein from SHR. Concluding, in SHR, the attenuation of Ang II-induced venoconstriction by COX metabolites and B2R may be involved in the local response to conserve the normal cardiac output in established hypertension. Taken together, our data indicate that different mechanisms are involved in the regulation of venous tonus of normotensive and hypertensive rats. These differences probably reflect distinct factors that influence arterial and venous bed in hypertension. The authors are grateful to Sonia Maria Rodrigues Leite and Marta Rodrigues da Silva from the Institute of Biomedical Sciences – USP for technical assistance.

Leave a Reply

Your email address will not be published. Required fields are marked *

*

You may use these HTML tags and attributes: <a href="" title=""> <abbr title=""> <acronym title=""> <b> <blockquote cite=""> <cite> <code> <del datetime=""> <em> <i> <q cite=""> <strike> <strong>