1995
DOI: 10.1152/ajplung.1995.268.3.l509
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In vivo treatment with endotoxin induces nitric oxide synthase in rat main pulmonary artery

Abstract: Our aim was to demonstrate increased NO activity from inducible NO synthase (iNOS) in pulmonary arteries (PA) from rats treated with endotoxin [lipopolysaccharide (LPS), 20 mg/kg ip]. LPS treatment diminished the contractile response of PA to potassium chloride (KCl) and phenylephrine (PE) and increased levels of guanosine 3',5'-cyclic monophosphate (cGMP) in endothelium-denuded vessels. Both the NO synthase (NOS) antagonists NG-monomethyl-L-arginine (L-NMMA; nonselective) and aminoguanidine (selective for iNO… Show more

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Cited by 49 publications
(44 citation statements)
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“…It is, therefore, likely that unstimulated basal production of NO in these vessels was due mainly to iNOS, which was at this time predominant in the endothelial cells. These results are consistent with previous data demonstrating induction of NOS both in endothelial and smooth muscle cell layers of PA from rats treated with endotoxin [19].…”
Section: Discussionsupporting
confidence: 93%
“…It is, therefore, likely that unstimulated basal production of NO in these vessels was due mainly to iNOS, which was at this time predominant in the endothelial cells. These results are consistent with previous data demonstrating induction of NOS both in endothelial and smooth muscle cell layers of PA from rats treated with endotoxin [19].…”
Section: Discussionsupporting
confidence: 93%
“…This difference could lead to hypocontractile response to histamine in mesenteric but not in pulmonary arteries. Our findings may provide a basis for the results of past investigations that iNOS induction-associated vascular hypocontractility was not observed in the pulmonary circulation (Nelson et al, 1991;Suba et al, 1992;Spath et al, 1994;Fullerton et al, 1995) despite the presence of iNOS mRNA in pulmonary vessels in vivo LPS (Griffiths et al, 1995).…”
Section: Vascular Hyporesponsiveness To Vasocontractile Stimulisupporting
confidence: 77%
“…Finally, iNOS deficient mice have been found to be resistant to vascular hypocontractility (Gunnett et al, 1998). Accordingly, iNOS, which generates large amounts of NO, is likely to be a critical mediator of the diminished vascular contractility in sepsis (Fleming et al, 1991;Griffiths et al, 1995;Hom et al, 1995).…”
Section: Vascular Hyporesponsiveness To Vasocontractile Stimulimentioning
confidence: 99%
“…50 LPS produces impaired eNOSdependent relaxation in vessels, 14,15,18 and expression of iNOS has been demonstrated in blood vessels after LPS. 3,4,9 Responses to pharmacological inhibitors, such as aminoguanidine, suggest that iNOS mediates impaired endothelial function after LPS. 12,20,21 However, inhibition of neuronal NO synthase also improves endothelium-dependent relaxation during inflammation.…”
Section: Effects Of Inos On Vasorelaxationmentioning
confidence: 99%
“…1,2 In general, proinflammatory stimuli produce the expression of iNOS within the vessel wall. [3][4][5][6][7][8] Expression of iNOS during systemic inflammation contributes to impaired contraction, 3,4,9,10 but effects of iNOS on vasorelaxation have not been clearly established. Several studies suggest that vasorelaxation is impaired after inflammatory stimuli, such as lipopolysaccharide (LPS), [11][12][13][14] but others report normal vasorelaxation after LPS.…”
mentioning
confidence: 99%