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1 Department of Biochemistry and Molecular Biology, New York Medical College, Valhalla, NY, USA
2 Department of Pathology, New York Medical College, Valhalla, NY, USA
3 Department of Pharmacology, New York Medical College, Valhalla, NY, USA
* To whom correspondence should be addressed. E-mail: susan_olson{at}nymc.edu.
We previously reported that angiotensin II stimulates an increase in nitric oxide production in pulmonary artery endothelial cells. The aims of this study were to determine which receptor subtype mediates the angiotensin II-dependent increase in nitric oxide production and to investigate the roles of the angiotensin type 1 and type 2 receptors in modulating angiotensin II-dependent vasoconstriction in pulmonary arteries. Pulmonary artery endothelial cells express both angiotensin II type 1 and type 2 receptors as assessed by reverse transcriptase polymerase chain reaction, Western blot analysis and flow cytometry. Treatment of the endothelial cells with PD123319, a type 2 receptor antagonist, prevented the angiotensin II-dependent increase in nitric oxide synthase mRNA, protein levels and nitric oxide production. In contrast, the type 1 receptor antagonist, losartan, enhanced nitric oxide synthase mRNA levels, protein expression and nitric oxide production. Pretreatment of the endothelial cells with either PD123319 or an anti-angiotensin II antibody prevented this losartan enhancement of nitric oxide production. Angiotensin II-dependent enhanced hypoxic contractions in pulmonary arteries were blocked by the type 1 receptor antagonist, candesartan; however, PD123319 enhanced hypoxic contractions in angiotensin II treated endothelial-intact vessels. These data demonstrate that angiotensin II stimulates an increase in nitric oxide synthase mRNA, protein expression and nitric oxide production via the type 2 receptor, whereas signaling via the type 1 receptor negatively regulates nitric oxide production in the pulmonary endothelium. This endothelial, type 2 receptor-dependent increase in nitric oxide may serve to counterbalance the angiotensin II-dependent vasoconstriction in smooth muscle cells, ultimately regulating pulmonary vascular tone.
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