Blood pressure and renal hemodynamic effects of angiotensin fragments

Angiotensin (Ang) II, the main effector peptide of the renin–Ang system, increases arterial blood pressure through Ang II type 1A (AT1a) receptor-dependent arterial vasoconstriction and by decreasing renal salt and water excretion through extrarenal and intrarenal mechanisms. AT2 receptors are assumed to oppose these responses mediated by AT1 receptors, thereby attenuating the pressor effects of Ang II. Nevertheless, a possible role of AT2 receptors in the regulation of renal hemodynamics and sodium homeostasis remains to be unclear. Several other Ang fragments such as Ang III, Ang IV, Ang-(1–7) and Ang A have also been shown to display biological activity. In this review, we focus on the effects of these Ang on blood pressure, renal hemodynamics and sodium water handling, and discuss the receptors involved in these actions.