Enhancement of phosphatidylcholine biosynthesis by angiotensin-(1–7) in the rat renal cortex

In the present paper, we investigated the effect of angiotensin-(1–7) (Ang-(1–7)) on phospholipid biosynthesis in the rat renal cortex. A significant increase in phosphatidylcholine (PC) labeling was observed when cortical slices, prelabeled with [ 32 P ]orthophosphate, were incubated for 30 min in the presence of Ang-(1–7) (1 pM to 100 nM). Neither the phospholipase C inhibitors, neomycin or db-cAMP nor the protein kinase C inhibitors, chelerythrine or H7, modified the stimulatory effect induced by 0.1 nM Ang-(1–7). The enhancement of PC biosynthesis caused by 0.1 nM Ang-(1–7) was unmodified by either losartan, an AT 1 receptor antagonist, or (1-[[4-(dimethylamino)-3-methylphenyl]methyl]-5-(diphenylacetyl)-4,5,6,7-tetrahydro-1 H-imidazol[4,5- c]pyridine-6-carboxylic acid ditrifluoroacetate) (PD 123319), an AT 2 receptor antagonist, but was partially blocked by [ d-Ala 7]Ang-(1–7), an Ang-(1–7) specific antagonist. However, losartan potentiated the effect of 100 nM Ang-(1–7) on PC biosynthesis. Losartan by itself increased the de novo synthesis of PC. These results suggest that the Ang-(1–7)-mediated increase in PC biosynthesis is independent of AT 1 and AT 2 receptor activation but mediated by a specific Ang-(1–7) receptor. This mechanism is independent of phospholipase C and PKC activation.