Role of nitric oxide in lipopolysaccharide-induced mortality from spontaneously hypertensive rats

摘要: Abstract To investigate whether nitric oxide (NO) contributed to a higher mortality induced by lipopolysaccharide (LPS) in spontaneously hypertensive rats (SHR), NO synthase inhibitors were used examine the from LPS SHR and normotensive Wistar-Kyoto (WKY) rats. We evaluated series of doses (5, 10, or 20 mg kg , i.v.) anesthetized rat. Plasma nitrite was measured before at 1, 2, 3 h after treated with (5 i.v.). Pressure responses Nω-nitro- l -arginine methyl ester ( -NAME) aminoguanidine (AG) performed without for h. Thoracic aortic cyclic guanosine 3′,5′-monophosphate (cGMP) levels also assessed. Our results demonstrated that injection caused dose-dependent both strains, having more marked effect SHR. The survival time much shorter A basal level plasma observed this difference further augmented LPS. administration -NAME (3 AG (15 had no significant effects on WKY rats, but significantly prolonged similar injecton prior increased blood pressure 28 ± 5 mmHg 38 4 mmHg. At LPS, greater pressor than By contrast, injected slightly 7 not 2 mmHg), whereas it In addition, cGMP which attenuated vitro treatment rings LPS-rats These suggest evoked is associated we propose elevated synthesis may play an important role compensatory mechanisms activated combat state.