Signal Transduction Mechanisms Involved in Angiotensin-(1–7)-Stimulated Arachidonic Acid Release and Prostanoid Synthesis in Rabbit Aortic Smooth Muscle Cells

摘要: This study investigated the signal transduction mechanisms of angiotensin-(1–7) [Ang-(1–7)]- and Ang II-stimulated arachidonic acid (AA) release for prostaglandin (PG) production in rabbit aortic vascular smooth muscle cells. II Ang-(1–7) enhanced AA cells prelabeled with [ 3 H]AA. However, 6-keto-PGF 1α synthesis produced by was much less than that caused Ang-(1–7). In presence lipoxygenase inhibitor baicalein, to a greater degree Angiotensin type (AT) 1 receptor antagonist DUP-753 inhibited only II-induced H]AA release, whereas AT 2 PD-123319 both II- Ang-(1–7)-induced release. d-Ala 7 -Ang-(1–7) effect Ang-(1–7), but not II. transiently transfected cytosolic phospholipase A (cPLA ), mitogen-activated protein (MAP) kinase or Ca ++ -/calmodulin-dependent (CAM) antisense oligonucleotides, Ang-(1–7)- attenuated. The CaM KN-93 MAP PD-98059 attenuated cPLA activity also increased activities. Although activity, did affect activity. Both translocation PLA nuclear envelope. These data show stimulate prostacyclin via activation distinct types receptors. peptides appear II, which turn, activation, enhances PG synthesis.