Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor.

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 RT-PCR, Western blot analysis, and flow cytometry.

Modulation of cGMP by human HO-1 retrovirus gene transfer in pulmonary microvessel endothelial cells.

Carbon monoxide (CO) stimulates guanylate cyclase (GC) and increases guanosine 3',5'-cyclic monophosphate (cGMP) levels. We transfected rat-lung pulmonary endothelial cells with a retrovirus-mediated human heme oxygenase (hHO)-1 gene. Pulmonary cells that expressed hHO-1 exhibited a fourfold increase in HO activity associated with decreases in the steady-state levels of heme and cGMP without changes in soluble GC (sGC) and endothelial nitric oxide synthase (NOS) proteins or basal nitrite production.

Roles for NAD(P)H oxidases and reactive oxygen species in vascular oxygen sensing mechanisms.

Observations that physiological levels of O2 control the rates of production of reactive O2 species by systems including NAD(P)H oxidases and that certain of these species have signalling mechanisms that regulate vascular tone has resulted in consideration of these systems in processes that mediate the sensing of changes in P(O2). Evidence exists for the participation of hydrogen peroxide-dependent regulation of prostaglandin production and soluble guanylate cyclase activity, resulting from the metabolism of peroxide by cyclooxygenase and catalase, respectively, in P(O2)-elicited signalling mechanisms that regulate vascular force generation. A microsomal NADH oxidase whose activity is controlled by the redox status of cytosolic NAD(H) appears to function as a P(O2) sensor in bovine pulmonary and coronary arteries where changes in O2 levels control the production of superoxide anion-derived hydrogen peroxide and a cGMP-mediated relaxation response.

ANG II stimulates endothelial nitric oxide synthase expression in bovine pulmonary artery endothelium.

Although angiotensin II (ANG II) is a known pulmonary vasoconstrictor, the purpose of this study was to examine the effect of ANG II on pulmonary artery endothelial cell nitric oxide synthase (ecNOS) mRNA and protein expression. Cultured bovine pulmonary artery endothelial (BPAE; passages 5-8) cells were incubated for 0-12 h with 10(-6) M ANG II. Total RNA was extracted, and ecNOS expression was assessed by Northern blot analysis.

Peripheral hypertension and alterations in pulmonary vascular regulation.

We have recently reported in normal isolated-perfused rat lungs that low basal tone appears to be regulated by nitric oxide (NO)-dependent and -independent mechanisms of soluble guanylate cyclase activation. In this study, we examined the role of NO in the regulation of pulmonary artery (PA) tone from rats with renin-dependent hypertension. Rats were made hypertensive by ligating the abdominal aorta above the left and below the right renal artery (aortic coarctation, AC).