25 a.u.; n = 5) ( Fig. 5). Ang II evoked a consistent constriction in mesenteric venules and portal vein from SHR. In both vascular preparations, losartan
reduced or nearly abolished the Ang II-mediated constriction, while PD123319 did not modify this response. Ang II-induced venoconstriction was markedly increased by indomethacin, while celecoxib was effective only in mesenteric venules. Whereas vascular responses to check details Ang II were augmented by HOE-140, L-NAME had no effect. By analyzing our results, we found that Ang II-induced constriction in mesenteric venules and portal vein from SHR is dependent of AT1R activation and counterbalanced by COX metabolites and kinin B2R. Several aspects of our results may point to important differences between the venous system of normotensive and hypertensive rats. For instance, Ang II-induced constriction was significantly attenuated in portal vein rings from SHR. Besides, Ang II-induced venoconstriction
was mediated by both AT1R and AT2R in normotensive rats . Considering SGI-1776 molecular weight these findings, we hypothesized that differences between strains could be related to changes in angiotensin receptors expression. In fact, when AT1R and AT2R were evaluated, the AT2R expression was significantly reduced in portal vein from SHR. Although several studies have investigated the influence of AT2R in the vascular system, the functional role of this subtype is not completely elucidated. Authors have demonstrated that AT2R activation can induce both vasodilation  and vasoconstriction  and . In this regard, a consistent vasoconstrictor effect of Ang II mediated by AT2R in mesenteric arterioles of SHR has been demonstrated  and . PIK3C2G Moreover, AT2R also participates of contractile effect of Ang II in portal vein preparations from normotensive rats  and . Probably, reduction of AT2R levels in
portal vein from SHR can be responsible for the decreased response observed by us. This result can indicate that AT2R plays a distinct role in the vasculature of normotensive and hypertensive rats. The basic hemodynamic disturbance in established hypertension is an elevation of total peripheral resistance, which is determined mainly by resistance vessels from arterial system. In fact, it is well established that hypertensive patients have similar values of cardiac output in comparison with normotensive controls and the elevated blood pressure is maintained by increase in total peripheral resistance  and . Similarly, it was demonstrated that cardiac output is not altered in SHR, a generally accepted model for human essential hypertension  and . From this point of view, reduced Ang II response observed in venous from SHR would not be influencing cardiac output control.