Oxidative stress hypertension

Wu, L., Ashraf, M.H., Facci, M., Wang, R., Paterson, P.G., Ferrie, A., and Juurlink, B.H. 2004. Dietary approach to attenuate oxidative stress, hypertension, and inflammation in the cardiovascular system. Proc Natl Acad Sci USA 101 7094-7099. 

Patients with CKD are at increased risk of cardiovascular disease, independent of the etiology of their kidney disease. While a clearly unique pathogenesis of cardiovascular disease specific to CKD has not been identified, it is known that manifestations of kidney disease are contributory. Risk factors for cardiovascular disease in this population include hemodynamic and metabolic abnormalities, as well as hypertension, dyslipidemia, elevated homocysteine levels, anemia, hyperparathyroidism, malnutrition, and oxidative stress. Hypertension induced by volume expansion and increased systemic vascular resistance increases myocardial work and contributes to development of left ventricular hypertrophy (LVH). Hyperlipidemia may enhance atherogenesis, while some uremic toxins can decrease myocardial contractflity. In addition, uremic toxins can induce pericarditis, a potentially fatal complication. Currently, measures to screen this high-risk population for cardiovascular risk factors are not routine. ... 

However, it remains a valid argument (as in the case of atheroma) that increased oxidative stress may be secondary to (rather than a cause of) endothelial damage in hypertension due to other mechanisms. 

The possible involvement of free radicals in the development of hypertension has been suspected for a long time. In 1988, Salonen et al. [73] demonstrated the marked elevation of blood pressure for persons with the lowest levels of plasma ascorbic acid and serum selenium concentrations. In subsequent studies these authors confirmed their first observations and showed that the supplementation with antioxidant combination of ascorbic acid, selenium, vitamin E, and carotene resulted in a significant decrease in diastonic blood pressure [74] and enhanced the resistance of atherogenic lipoproteins in human plasma to oxidative stress [75]. Kristal et al. [76] demonstrated that hypertention is accompanied by priming of PMNs although the enhancement of superoxide release was not correlated with the levels of blood pressure. Russo et al. [77] showed that essential hypertension patients are characterized by higher MDA levels and decreased SOD activities. 

Wassmann S, Laufs U, Stamenkovic D, Linz W, Stasch JP, Ahlbory K, Rosen R, Bohm M, Nickening G (2002) Raloxifene improves endothelial dysfunction in hypertension by reduced oxidative stress and enhanced nitric oxide production. Circulation 105 2083-2091... 

Epidemiologic, experimental, and in vitro mechanistic data indicate that lead exposure elevates blood pressure in susceptible individuals. In populations with environmental or occupational lead exposure, blood lead concentration is linked with increases in systolic and diastolic blood pressure. Studies of middle-aged and elderly men and women have identified relatively low levels of lead exposure sustained by the general population to be an independent risk factor for hypertension. In addition, epidemiologic studies suggest that low to moderate levels of lead exposure are risk factors for increased cardiovascular mortality. Lead can also elevate blood pressure in experimental animals. The pressor effect of lead may be mediated by an interaction with calcium mediated contraction of vascular smooth muscle, as well as generation of oxidative stress and an associated interference in nitric oxide signaling pathways. 

The human reproductive process does not fit perfectly into the animal model of reproductive and developmental toxicity. Conditions of the fetal-maternal unit that affect both mother and child have not been adequately addressed in this monograph, although there is some evidence that some of these adverse outcomes, such as pregnancy-induced hypertension, may be related to environmental exposure (Tabacova et al., 1998 Dawson et al., 1999). This is a promising frontier for new research. We have also not dealt with genetic susceptibility to developmental toxicants. Advances in this field may illuminate many of the mysteries of how toxicants act, and on whom. Limited data are available on mechanisms of action (see section 5.2.4). The work on oxidative stress in pregnancy (Tabacova et al., 1998 Hubei,... 

Reckelhoff JF, Romero JC. 2003. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol 284 R893-912. 

Cardiovascular diseases, such as hypertension, coronary heart disease (CHD), and atherosclerosis, are associated with increased oxidative stress and are more common in men than in premenopausal women of similar age, with the incidence of CHD increasing significantly after menopause, with loss of cardiovascular protection attributed to estrogen deficiency [Forte et al., 1998]. Differences in the regulation of blood pressure and vascular function between males and females have been investigated extensively over the past... 

Friedman, J., Peleg, E., Kagan, T., Shnizer, S., and Rosenthal, T. 2003. Oxidative stress in hypertensive, diabetic, and diabetic hypertensive rats. Am. J. Hypertens. 16, 1049-1052. 

Paran, E. and Engelhard, Y. 2001. Effect of Lyc-O-Mato, standardized tomato extract on blood pressure, serum lipoproteins, plasma homocysteine and oxidative stress markers in grade 1 hypertensive patients. In Proceedings of the 16th Annual Scientific Meeting of the Society of Hypertension , San Francisco, USA. 

Diep QN, Amiri F, Touyz RM, et al. PPARalpha activator effects on Ang Il-induced vascular oxidative stress and inflammation. Hypertension 2002 40 866-871. 

Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats.

Takimoto, E., and Kass, D.A. 2007. Role of oxidative stress in cardiac hypertrophy and remodeling. Hypertension 49 241-248. 

Tanito, M., Nakamura, H., Kwon, Y.W., Teratani, A., Masutani, H., Shioji, K., Kishimoto, C., Ohira, A., Horie, R., and Yodoi, J. 2004. Enhanced oxidative stress and impaired thioredoxin expression in spontaneously hypertensive rats. Antioxid. Redox Signal. 6 89-97. 

Vaziri, N.D., Wang, X.Q., Oveisi, F., and Rad, B. 2000. Induction of oxidative stress by glutathione depletion causes severe hypertension in normal rats. Hypertension 36 142-146. 

Wu, L., and Juurlink, B.H. 2002. Increased methylglyoxal and oxidative stress in hypertensive rat vascular smooth muscle cells. Hypertension 39 809-814. 

Increased levels of ROS due to oxidative stress have been consistently found in cardiovascular diseases as atherosclerosis or hypertension [18]. There is certain evidence that the free radicals involved in Parkinson s disease are mainly due to the production of increased levels of free radicals during oxidative metabolism of dopamine [19]. Oxidative stress, manifested by protein oxidation and lipid peroxidation (LP), among other alterations, is a characteristic of Alzheimer s disease [20] and in the pathogenesis of diabetes related complications. Treatment with antioxidants seemed to be a promising therapeutic option for these diseases [21], The inflammatory nature of rheumatoid arthritis implies that a state of oxidative stress may also exist in this disease [22,23]. Also, free radicals have a certain role in Huntington s disease [24,25], age related degeneration [26], and some autoimmune disorders [27],... 

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