Effects of antihypertensive agents, alpha receptor blockers, beta blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and calcium channel blockers, on oxidative stress

Background Free oxygen radicals and insufficiency of antioxidant enzymes have been implicated in the pathogenesis of hypertension disease (HD). Trace elements function as a co-factor in antioxidant enzymes. The antioxidant system and trace elements have been investigated in many different studies including HD, but these subjects have not been investigated as a whole in these patients. Objective The aim of the present study was to investigate the antioxidative system and trace elements in hypertensive patients given different antihypertensive therapy. Methods We examined malondialdehyde and superoxide dismutase activities together with copper and zinc levels in plasma of 102 patients with HD and in 51 healthy controls. Results It was found that in patients with HD, plasma malondialdehyde was significantly higher than those of controls, while plasma superoxide dismutase activities were significantly lower in patients with HD. Plasma zinc levels were significantly higher than those of controls and plasma copper levels were significantly lower in patients with HD. Plasma lipid levels and oxidative state were analyzed in five different treatment groups given antihypertensive drug therapy before and after a 3-month treatment period. Conclusions In conclusion, our clinical study shows that angiotensin-converting enzyme inhibitors and angiotensin receptor blockers have notable effects on oxidative stress, and are an essential step in managing essential hypertension by the way of improvement of endothelial dysfunction. Although it has been shown that calcium channel blockers, beta blockers and alpha receptor blockers have antioxidant effects in in vitro conditions, we did not demonstrate these effects in our clinical study.

[1]  Cathy Theresa Thomas.  Trace elements. , 2013, Lancet.

[2]  T. Lüscher,et al.  Vascular Effects of Newer Cardiovascular Drugs: Focus on Nebivolol and ACE‐Inhibitors , 2001, Journal of cardiovascular pharmacology.

[3]  A. Dominiczak,et al.  Renin angiotensin system inhibition is associated with reduced free radical concentrations in arteries of patients with coronary heart disease , 2001, Heart.

[4]  J. Redón,et al.  P-653: Oxidative stress and enzymatic antioxidant mechanisms in essential hypertension , 2001 .

[5]  H. Drexler,et al.  Comparative Effect of ACE Inhibition and Angiotensin II Type 1 Receptor Antagonism on Bioavailability of Nitric Oxide in Patients With Coronary Artery Disease: Role of Superoxide Dismutase , 2001, Circulation.

[6]  G. Sahin,et al.  Oxidative stress and nitric oxide related parameters in type II diabetes mellitus: effects of glycemic control. , 2001, Clinical biochemistry.

[7]  K. Kędziora-Kornatowska,et al.  Effect of angiotensin convertase inhibitors and AT1 angiotensin receptor antagonists on the development of oxidative stress in the kidney of diabetic rats. , 1999, Clinica chimica acta; international journal of clinical chemistry.

[8]  S. Toyokuni.  Reactive oxygen species‐induced molecular damage and its application in pathology , 1999, Pathology international.

[9]  J. Knight.  Free radicals: their history and current status in aging and disease. , 1998, Annals of clinical and laboratory science.

[10]  B. Tomlinson,et al.  Antioxidant power of angiotensin-converting enzyme inhibitors in vitro. , 1998, British journal of clinical pharmacology.

[11]  L. Raij,et al.  Effect of doxazosin on endothelial dysfunction in hypercholesterolemic/antioxidant-deficient rats. , 1997, American journal of hypertension.

[12]  J. Keaney,et al.  Antioxidants and atherosclerotic heart disease. , 1997, The New England journal of medicine.

[13]  G. Feuerstein,et al.  Carvedilol, a novel vasodilating beta-blocker with the potential for cardiovascular organ protection. , 1996, European heart journal.

[14]  B. Frei.  Reactive oxygen species and antioxidant vitamins: mechanisms of action. , 1994, The American journal of medicine.

[15]  J. Mckenney,et al.  Summary of the second report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel II) , 1993, JAMA.

[16]  J. Néve,et al.  Methods in determination of selenium states. , 1991, Journal of trace elements and electrolytes in health and disease.

[17]  S. Jain,et al.  Hyperglycemia can cause membrane lipid peroxidation and osmotic fragility in human red blood cells. , 1989, The Journal of biological chemistry.

[18]  M. L. Kennedy,et al.  Influence of genetic obesity on tissue concentrations of zinc, copper, manganese and iron in mice. , 1986, The Journal of nutrition.

[19]  W. Weglicki,et al.  Differential Sensitivity of Canine Cardiac Sarcolemmal and Microsomal Enzymes to Inhibition by Free Radical‐Induced Lipid Peroxidation , 1984, Circulation research.

[20]  V. Nair,et al.  Novel adducts from the modification of nucleic acid bases by malondialdehyde , 1984 .

[21]  G. R. Tudhope,et al.  Glutathione Peroxidase in Human Red Cells in Health and Disease , 1973, British journal of haematology.

[22]  L. Ghiadoni,et al.  Effects of antihypertensive drugs on endothelial dysfunction: clinical implications. , 2002, Drugs.

[23]  M. Luyckx,et al.  Effects of two antihypertensive agents, labetalol and metoprolol, on the production of reactive oxygen species by normal polymorphonuclear leukocytes in vitro. , 1999, Hypertension in pregnancy.

[24]  R. Weinshilboum,et al.  The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure. , 1997, Archives of internal medicine.

[25]  N. Seidler,et al.  Exercise causes oxidative damage to rat skeletal muscle microsomes while increasing cellular sulfhydryls. , 1994, Life sciences.