The aim of this study was to analyze the effect of vitamins C and E on malondialdehyde (MDA) content and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) as well as glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. Wistar male rats were divided into following groups (12 rats each): the control, diabetic rats, diabetic rats whose drinking water was supplemented with vitamin C in a dose of 1.0 g/l or diet was supplemented with 200 mg of vitamin E/100 g fodder. Body weight, blood glucose and HbA1C levels and 24-hour urinary albumin excretion (UAE) were studied every week (0–12 weeks). After 6 and 12 weeks, MDA content and activities of SOD, CAT and GSH-Px were measured in the kidney homogenate supernatants. Electron micrographs of glomeruli were scanned and morphometric investigations were performed by means of computer image analysis system to compare GBM thickness. The blood glucose and HbA1C concentrations and UAE in diabetic rats were significantly higher than in the control group. An increase in the MDA level and decrease in the SOD, CAT and GSH-Px activities in the kidney of diabetic rats were observed after 6 and 12 weeks of experiment. Administration of vitamins C and E did not affect body weight, blood glucose and HbA1C levels. Both vitamin C and vitamin E decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of diabetic rats as well as reduced UAE, decreased kidney weight and GBM thickness. The results indicate the potential utility of antioxidant vitamins in the protection against the development of diabetic nephropathy.

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Vascular smooth muscle tone changes under the influence of numerous contracting and relaxing factors. The purpose of the present study was to determine the modulating effect of ischemia and reperfusion (I/R) on contraction triggered by angiotensin II (ANG II) and Bay K8644 as well as to investigate the importance of nitric oxide (NO) and cGMP in these reactions. Experiments were performed on isolated and perfused Wistar rat tail arteries. The contraction triggered by ANG II and Bay K8644 with the use of intracellular (in calcium-free physiological salt solution; FPSS) and extracellular (in physiological salt solution; PSS) pools of calcium ions after I/R and in the presence of sodium nitroprusside (SNP), 8Br-cGMP, an endothelial NO synthase (NOSe) inhibitor (L-NG-nitroarginine methyl ester; L-NAME) or ODQ [an inhibitor of soluble guanylyl cyclase (GC)] was evaluated. ANG II triggered contraction in FPSS and PSS, but Bay K8644 only in PSS. Ischemia reduced and reperfusion intensified the response of the artery to ANG II, but did not change the action of Bay K8644. SNP and 8Br-cGMP reduced the response of the vessels to ANG II and did not change the modulating effect of ischemia, but reduced the intensifying action of reperfusion on contraction caused by the presence of ANG II. SNP lowered the action of Bay K8644 in PSS. In PSS, L-NAME and ODQ intensified the action of ANG II, eliminating the reducing effect of ischemia on the contraction caused by ANG II, but did not influence the intensifying reaction caused by reperfusion. L-NAME and ODQ did not influence the action of Bay K8644. I/R modulated the contraction of arteries triggered by ANG II, but did not influence the response to Bay K8644. The intra- and extracellular pools of calcium ions mediate the action of ANG II, but Bay K8644 stimulated contraction only with participation of calcium ions flowing into the cell. Control of the vascular smooth muscle tone associated with the action of NO and cGMP is subject to modulation under conditions of I/R.

1. The aim of the present study was to determine the effect of hypotensive therapy with a diuretic (hydrochlorothiazide) and an angiotensin-converting enzyme inhibitor (perindopril) on selected oxidative stress parameters in the blood of elderly patients with essential hypertension. 2. Studies were performed in 45 elderly patients with essential hypertension at baseline and after the 45th day of perindopril (n = 25) or hydrochlorothiazide (n = 20) therapy, as well as in 25 young and 25 elderly normotensive subjects. The following parameters were measured: systolic and diastolic blood pressure, nitric oxide (NO), carbonyl groups and malondialdehyde (MDA) concentrations, as well as the activity of ceruloplasmin (Cp) oxidase, Cu-Zn superoxide dismutase (SOD-1) and catalase (CAT). 3. The activity of SOD-1 and NO levels were reduced with age. 4. Compared with elderly controls, hypertensive subjects showed increases in baseline MDA, carbonyl group concentrations and Cp oxidase activity and decreases in NO levels and SOD-1 and CAT activities. 5. Treatment with perindopril, but not hydrochlorothiazide, resulted in significant increases in SOD-1 and CAT activities and decreases in MDA concentration and Cp oxidase activity. Both therapies decreased the level of carbonyl groups and increased NO levels. 6. Angiotensin-converting enzyme inhibitor therapy has significant anti-oxidant effects that may be important in the treatment of elderly patients with essential hypertension.

Abstract. The aim of this study was to determine the role of acetylcholine and calcium ions in modulating the vascular contraction induced by angiotensin II (ANG II), phenylephrine (PHE) and caffeine. The study was performed on perfunded Wistar rat tail arteries. The contraction caused by ANG II, PHE and caffeine with the participation of intracellular [in free physiological salt solution (FPSS)] and extracellular [in physiological salt solution (PSS), after emptying the cellular stores] pools of calcium ions and the addition of L-NNA (NOSe inhibitor) or ODQ (GC inhibitor) was studied. Then the effect of acetylcholine on the contraction responses was analyzed. ANG II, PHE and caffeine induced an increase in perfusion pressure in PSS and FPSS. Acetylcholine reduced the contraction resulting from the presence of ANG II and PHE, but not caffeine. L-NNA and ODQ abolished the spasmolytic action of acetylcholine. Both pools of calcium ions mediated the action of ANG II and PHE, and caffeine induced the contraction with the participation of calcium released from intracellular stores. The spasmolytic effect of acetylcholine on responses stimulated by ANG II and PHE indicates the participation of nitric oxide in modulating the reactivity of the arteries on the studied agonists of the metabotropic receptors. No observed acetylcholine effect on caffeine suggests that the pathway associated with nitric oxide does not interfere with the contraction induced by the ryanodin receptor.