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• W2061928914 abstract "The heptapeptide, angiotensin-(1–7), is an active member of the renin–angiotensin system. The present study was designed to characterize the role of endothelium in relaxations of large cerebral arteries to angiotensin-(1–7). Rings of canine middle cerebral arteries were suspended in organ chambers for isometric force recording. The levels of cyclic guanosine 3′,5′-monophosphate (cGMP) were assessed by radioimmunoassay. During contraction to uridine 5′-triphosphate (UTP, 3×10−6 to 10−5 mol/l), angiotensin-(1–7) (10−9 to 3×10−5 mol/l) caused concentration-dependent relaxations in arteries with endothelium, but not in endothelium-denuded vessels. Angiotensin-(1–7) significantly increased formation of cGMP. Nitric oxide synthase inhibitor, N-ω-nitro-l-arginine methyl ester (l-NAME, 3×10−4 mol/l), and selective soluble guanylate cyclase inhibitor, 1 H-[1,2,4]oxadiazolo[4,3-a]quinozalin-1-one (ODQ, 3×10−6 mol/l), abolished angiotensin-(1–7)-induced relaxations. Angiotensin receptor antagonists, losartan (10−5 mol/l), PD 123 319 (10−5 mol/l), [Sar1,Thr8]-angiotensin II (10−5 mol/l) [Sar1,Val5,Ala8]-angiotensin II (10−5 mol/l) or [7-d-Ala]-angiotensin 1–7 (10−6 mol/l) did not affect these relaxations. However, angiotensin-converting enzyme inhibitor, captopril (10−5 mol/l) augmented relaxations to angiotensin-(1–7). Finally, bradykinin B2 receptor antagonist, [d-Arg0,Hyp3,Thi5,d-Tic7,Oic8]-bradykinin (HOE 140, 5×10−8 mol/l) significantly reduced the effect of angiotensin-(1–7), while bradykinin B1 receptor antagonist, des-Arg9, [Leu8]-bradykinin (6×10−9 mol/l) did not influence the vascular response to the heptapeptide. These findings indicate that (1) angiotensin-(1–7) produces relaxation of canine middle cerebral arteries by the release of nitric oxide from endothelial cells, (2) angiotensin receptors do not mediate endothelium-dependent relaxations to the heptapeptide, and (3) this effect appears to be dependent on activation of local production of kinins. Our studies support the concept that angiotensin-(1–7), as a natural vasodilator hormone, may counterbalance the hemodynamic actions of angiotensin II." @default.
• W2061928914 created "2016-06-24" @default.
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• W2061928914 date "2000-08-01" @default.
• W2061928914 modified "2023-10-01" @default.
• W2061928914 title "Angiotensin-(1–7) causes endothelium-dependent relaxation in canine middle cerebral artery" @default.
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• W2061928914 doi "https://doi.org/10.1016/s0006-8993(00)02482-3" @default.
• W2061928914 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10915812" @default.
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