Interactions between angiotensin II and phenylephrine on isolated rat renal arteries and veins.

It is know that not only decreased blood flow to the kidney but also obstruction of renal outflow may, in some instances, be a cause of hypertension. In this view were compared angiotensin (Ang) II responses and investigated interactions between Ang II and phenylephrine (Phe) on renal vessels. Studies were performed on renal artery and vein rings without endothelium obtained from young (4 months) and old (12 month of age) male Wistar rats. As compared with control contractions (40 microM KC1) there are no differences between renal artery and veins on Phe- or Ang II-induced contractions. Phe -induced contractions after 1 microM Ang II pretreatment were higher on renal veins than arteries. Ang II administered after 1 microM Phe could additional increase Phe-induced contractions only on renal veins. On the other hand, these differences between renal arteries and veins responses were significantly higher on rings obtained from old as compared those from young rats. These age-dependent differences between renal artery and vein reactivity can be a possible cause of input-output renal blood flow unbalance and might become important in some pathological states which associate sympathetic activation with hyperreninemia.

Are multiple angiotensin receptor types involved in angiotensin (1-7) actions on isolated rat portal vein.

Angiotensin (1-7) [Ang (1-7)] is a bioactive component of the renin angiotensin system. Ang (1-7) may interact with angiotensin type 1 (AT1) or type 2 (AT2) receptors and with Ang (1-7) - specific receptors. We examined the interactions between different doses of Ang (1-7) (1 nM-1 microM) and angiotensin II (Ang II) (10 and 100 nM) on isolated rat portal vein. In endothelium-denuded portal vein rings, Ang (1-7) inhibited contractile effects induced by Ang II. The effects of Ang (1-7) were modified by indomethacin, N(G)-nitro-L-arginine methyl ester (L-NAME), (D-Ala7)-Angiotensin (1-7) (H-2888) and losartan. Our results suggest that on rat isolated portal vein rings without endothelium, Ang (1-7) reduces Ang II-induced contractions by acting mostly on Ang (1-7) specific receptors, and this effect is mediated by vasodilatatory prostaglandins. At high concentrations, Ang (1-7) effects are mediated by AT1-receptors, though to a lesser extent than by Ang (1-7) specific receptors.