Hypertension : Does Impaired Endothelium-Dependent Relaxation Affect Superoxide Scavenging?

Abstract

The purpose of this study was to investigate the effects of acute nitric oxide synthase inhibition on mean arterial blood pressure, oxidative stress markers such as plasma malondialdehyde (MDA) concentration, intracellular antioxidant enzyme activities such as copper-zinc superoxide dismutase (Cu/Zn SOD) and catalase and on trace elements important for activity and stability of Cu/Zn-SOD. Wistar-Kyoto rats (approx 150 g) (n=11) were treated with Nomega-nitro-L-arginine methyl esther (L-NAME) (0.5 mg/mL) for 2 d. Age- and bodyweight-matched rats (n=10) were used for control group. Their systolic blood pressures and heart rates were recorded daily during the experimental period and also before their blood samples were drawn. Plasma MDA, plasma and red cell zinc and copper concentrations, and red cell Cu/Zn-SOD and catalase activities were determined. A progressive rise in systolic arterial blood pressure was observed compared to the control group (p<0.001). The heart rate of the experimental group was reduced on the third day (p<0.05). Plasma MDA concentration and red cell catalase activity were increased in the experimental group (p<0.001 and p<0.001, respectively). Plasma copper and red cell zinc concentrations were also increased significantly in the experimental group (p<0.001 and p<0.01, respectively). In conclusion, impairment in endothelium-derived relaxation altered mean arterial blood pressure, oxidant status, and trace element concentrations.

Impaired Vasodilation in the Pathogenesis of Hypertension: Focus on Nitric Oxide, Endothelial‐Derived Hyperpolarizing Factors, and Prostaglandins

“…Collectively, these actions reduce cardiac hemodynamic load, thereby reducing myocardial hypertrophy and left ventricular dysfunction and protecting target organs 11–15 . Thus, NO plays a major role in maintaining and regulating BP 16–20 …”

Role of Zinc in Hemostasis: A Review

“…Both zinc insufficiency and excess result in impaired function of copper-and zincdependent superoxide dismutase, which in turn can impair endothelium-dependent relaxation of vessels [56][57][58][59]. Zinc deficiency intensifies hypertension in spontaneously hypertensive rats (SHR), but not normotensive rats, whose blood pressure is increased by large zinc intake [57][58][59][60].…”

“…Zinc deficiency intensifies hypertension in spontaneously hypertensive rats (SHR), but not normotensive rats, whose blood pressure is increased by large zinc intake [57][58][59][60]. These results are linked to Cu/Sn SOD, suggesting that modulation of zinc-dependent endothelium function will indirectly affect the blood clotting and fibrinolysis processes by affecting the endothelium-serum-platelets interaction.…”

Zinc Supplementation or Regulation of its Homeostasis: Advantages and Threats

“…The efficiency of homeostatic mechanisms that prevent zinc deficiency or excessive zinc accumulation in the organism is genetically conditioned [21][22][23][24][25][32][33][34][35][36]. The genetic diversity of the population and zinc content in the diet may be determinants in the evolution of arterial hypertension or arteriosclerosis.…”