BACKGROUND: The aim of this study was to assess the effects of N-acetylcysteine (NAC) on nitric oxide and adrenergic pathways in mesenteric artery from spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY). METHODS: Rats were treated with 4 g x kg(-1) x day(-1) of NAC during 4 weeks or mesenteric beds were treated with 10 mmol/L of NAC during 20 min. RESULTS: In conscious rats, the NAC treatment produced a significant reduction of mean arterial pressure (MAP) and heart rate in SHR (P <.001). N(omega)-nitro-L-arginine methyl ester (L-NAME) caused a MAP increase in NAC-treated SHR of magnitude similar to that in WKY, which was significantly higher than that observed in control untreated SHR (P <.05). Chronic treatments with NAC improved the maximal relaxation of mesenteric arteries to A23187 in SHR (P <.001). Acute NAC treatment in vitro induced a vasodilation in Phe preconstricted arteries (P <.001) that was stronger in SHR than in WKY (P <.05) and was not abolished by L-NAME. The vasoconstrictory response and increases in inositol phosphate production induced by superoxide anion were attenuated by NAC treatment through its superoxide scavenging properties. In contrast, chronic and acute NAC treatments did not alter the vasodilatory response to beta-adrenergic receptor stimulation. CONCLUSIONS: The increase in NO-mediated vasodilator tone and the possible decrease in adrenergic vasoconstriction induced by NAC treatment in SHR could explain the hypotensive effect of NAC in this model of hypertension.
BACKGROUND: The aim of this study was to assess the effects of N-acetylcysteine (NAC) on nitric oxide and adrenergic pathways in mesenteric artery from spontaneously hypertensiverats (SHR) and Wistar-Kyoto rats (WKY). METHODS:Rats were treated with 4 g x kg(-1) x day(-1) of NAC during 4 weeks or mesenteric beds were treated with 10 mmol/L of NAC during 20 min. RESULTS: In conscious rats, the NAC treatment produced a significant reduction of mean arterial pressure (MAP) and heart rate in SHR (P <.001). N(omega)-nitro-L-arginine methyl ester (L-NAME) caused a MAP increase in NAC-treated SHR of magnitude similar to that in WKY, which was significantly higher than that observed in control untreated SHR (P <.05). Chronic treatments with NAC improved the maximal relaxation of mesenteric arteries to A23187 in SHR (P <.001). Acute NAC treatment in vitro induced a vasodilation in Phe preconstricted arteries (P <.001) that was stronger in SHR than in WKY (P <.05) and was not abolished by L-NAME. The vasoconstrictory response and increases in inositol phosphate production induced by superoxide anion were attenuated by NAC treatment through its superoxide scavenging properties. In contrast, chronic and acute NAC treatments did not alter the vasodilatory response to beta-adrenergic receptor stimulation. CONCLUSIONS: The increase in NO-mediated vasodilator tone and the possible decrease in adrenergic vasoconstriction induced by NAC treatment in SHR could explain the hypotensive effect of NAC in this model of hypertension.
Authors: Bulent Ergin; Philippe Guerci; Lara Zafrani; Frank Nocken; Asli Kandil; Ebru Gurel-Gurevin; Cihan Demirci-Tansel; Can Ince Journal: Intensive Care Med Exp Date: 2016-09-26