thiobarbituric-acid and Hypertension

Lipid peroxides and fluorescent serum proteins, possible markers of free radical activity, are increased in diabetic patients, particularly those with angiopathy. Captopril, an angiotensin converting enzyme (ACE) inhibitor, scavenges free radicals in vitro independently of ACE inhibition. This is probably due to the presence of a sulphydryl group which is not present in other ACE inhibitor drugs. We have compared the effects of captopril and enalapril on free radical activity in thirty-two diabetic subjects with hypertension (BP greater than 160/95 mmHg). After a three week run-in period on no antihypertensive therapy, patients were randomly allocated to receive captopril or enalapril, the dose titrated according to BP response. After three months, BP was well controlled in both groups and glycaemic control unchanged. Both drugs were associated with a reduction of fluorescent IgG (captopril:Baseline [BL] 0.564 vs. 12 weeks [w] 0.428, P less than 0.05, enalapril:BL 0.603 vs. 12w 0.422 P less than 0.05) and thiobarbituric acid reactive material (captopril:BL 2.35 nmol MDA vs. 12w 1.46 nmol, P less than 0.05, enalapril:BL 2.44 nmol vs. 12w 1.72 nmol, P less than 0.01). In contrast to in vitro studies, there was no significant difference between the drugs when used in therapeutic doses, questioning a hypothesised advantage of captopril over enalapril.

Topics: Adult; Aged; Blood Proteins; Captopril; Diabetes Mellitus, Type 2; Enalapril; Female; Free Radical Scavengers; Free Radicals; Humans; Hypertension; Lipid Peroxides; Male; Middle Aged; Thiobarbiturates

Early studies by our group have shown that lead-induced hypertension (HTN) is closely related to enhanced activity of reactive oxygen species (ROS). In addition, we have found indirect evidence that hydroxyl radical may be the most likely culprit in lead-exposed animals. In the present study, rat aortic endothelial cells were incubated in the presence of 0, 0.01, 0.1, 0.5, and 1.0 ppm lead acetate for 1, 24, and 48 h. At the conclusion of the incubation period cells were harvested and the media were collected. Lipid peroxidation products were measured as malondialdehyde-thiobarbituric acid (MDA-TBA) in the medium and hydroxyl radical was measured as 2,3-dihydroxybenzoic acid (2,3 DHBA) in the cells. After exposure to lead for 48 h, MDA-TBA generation and 2,3 DHBA formation were significantly increased. These data clearly demonstrate that lead exposure promotes hydroxyl radical generation and induces oxidative stress in isolated endothelial cells, mimicking the effects observed in lead-exposed animals. Enhanced inactivation of endothelium-derived nitric oxide by locally produced oxygen free radicals could contribute to endothelial dysfunction and HTN in lead-exposed animals.

Topics: Animals; Aorta, Thoracic; Cell Count; Cell Survival; Cells, Cultured; Culture Media; Endothelium, Vascular; Hydroxybenzoates; Hydroxyl Radical; Hypertension; Lead; Lipid Peroxidation; Malondialdehyde; Rats; Rats, Sprague-Dawley; Thiobarbiturates

This study was designed to investigate the alterations in thiobarbituric acid reactants (TBA-reactants) and enzymatic and nonenzymatic antioxidant levels induced by dexamethasone (Dex) in heart and kidney and to find out whether these alterations induced by Dex and its hypertensive effect had any role in the maintenance of hypertension in this model. Administration of dexamethasone induced severe loss of body weight, significant increase in heart and kidney weights and also marked electrocardiographic changes. The protein content in heart and kidney increased significantly during Dex administration and returned to near normalcy after withdrawal. Total activity of lactate dehydrogenase showed a significant increase in heart till day 8 of treatment, whereas in serum, it exhibited a significant decrease. The activity of CK in heart showed an increase till day 8 of treatment and approached normalcy thereafter. In serum, CK exhibited a decrease till day 8, remaining insignificant thereafter. CKMB in heart showed an insignificant increase initially, reaching normal levels on Dex withdrawal, whereas in serum, it showed a significant decrease throughout the experimental period. Mean arterial pressure (MAP) and heart rate increased significantly, while a significant elevation in the ST segment was noticed during administration as well as after withdrawal of Dex. The TBA-reactants levels were found to increase in heart and kidney during days 12 and 16 of administration with Dex and even after withdrawal of Dex, the levels were insignificantly elevated. The level of glutathione in heart and kidney increased from day 4 onwards and reached normalcy during the later stages of treatment and after withdrawal of Dex. The total sulfhydryl groups exhibited a significant increase in both heart and kidney throughout the experiment. The antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase exhibited a significant decrease in heart during Dex administration whereas, in kidney, they exhibited a significant increase during treatment and after withdrawal of Dex. Thus, Dex induced rise in mean arterial pressure, significant alterations in electrocardiographic parameters and also marked alterations in enzymatic and nonenzymatic antioxidant levels and in the TBA-reactants level in heart and kidney.

Topics: Animals; Antioxidants; Blood Pressure; Body Weight; Dexamethasone; Electrocardiography; Glucocorticoids; Glutathione; Heart; Hypertension; Kidney; Male; Myocardium; Organ Size; Proteins; Rats; Rats, Wistar; Sulfur; Thiobarbiturates

We examined the effect of high potassium (K) diet on oxidative stress to endothelium in hypertensive rats. Five-week-old stroke-prone spontaneously hypertensive rats (SHRsp) were fed a 5% high NaCl diet containing either 0.5% normal K (n = 28) or 2.1% high K (n = 19) for 6 weeks, and lipid peroxides in the aortic intima and plasma were measured. Lipid peroxides were extracted into an organic solvent to avoid the interference of carbohydrates or glycoproteins, and malondialdehyde (MDA) produced from lipid peroxides by acid-heating was measured by its reaction to thiobarbituric acid. The antioxidant butylated hydroxytoluene prevented spurious lipid peroxide formation during the whole procedure, and optimum Fe3+ allowed a maximum MDA production from lipid peroxides. The high K SHRsp showed lower lipid peroxide levels than the normal K SHRsp both in the intima (5.6 +/- 0.3 vs. 7.2 +/- 0.4 nmol MDA/mg fatty acids, p < 0.003) and plasma (0.91 +/- 0.08 vs. 1.46 +/- 0.10 nmol MDA/ml, p < 0.001). Mean arterial pressure was slightly lower by 13 mmHg in the high K SHRsp, but these differences were still obvious even when we compared groups of rats with precisely matching blood pressures. These results indicate that high K diets reduce oxidative stress on the endothelium of high NaCl-fed SHRsp independently of blood pressure changes. This effect may be involved in the mechanism by which high K diets protect endothelium and reduce stroke incidence in hypertensive animals. Thus, we improved the method of lipid peroxide measurement and propose the protective effects of high K diet against oxidative stress to endothelium in hypertension animals.

Topics: Animals; Antioxidants; Blood Vessels; Butylated Hydroxytoluene; Cerebrovascular Disorders; Endothelium, Vascular; Ferric Compounds; Genetic Predisposition to Disease; Hypertension; Lipid Peroxides; Male; Malondialdehyde; Oxidative Stress; Potassium, Dietary; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Thiobarbiturates; Tunica Intima

Serum concentrations of thiobarbituric acid reagible substance (TBARS) as indicator of lipid peroxidation, alpha-tocopherol and selen have been investigated in women with normal pregnancy and patients suffered from pregnancy-induced hypertension. In the group of patients with pregnancy-induced hypertension we observed an increase in serum concentration of TBARS, where as the serum concentrations of alpha-tocopherol and selen were unchanged. There was no correlation between increase in TBARS concentration and the severity of hypertension.

Topics: Blood Pressure; Female; Free Radicals; Gestational Age; Humans; Hypertension; Infant, Newborn; Lipid Peroxidation; Pre-Eclampsia; Pregnancy; Selenium; Thiobarbiturates; Vitamin E

Eight bulls and steers (research animals) and 18 bulls (surgical patients) were anesthetized with guaifenesin and thiopental or thiamylal and for 90 minutes with halothane. Arterial blood pressure and heart rate were recorded in all animals. Cardiac output, plasma glucose and lactate concentrations, PCV, plasma proteins and plasma thromboxane B2 values were determined before (control) and every 15 minutes during anesthesia in the research animals. Plasma catecholamine concentrations were measured in 3 of the research animals and 3 of the surgical patients. Arterial pressure, heart rate, and plasma thromboxane B2 and catecholamine concentrations were also measured immediately after the trachea was intubated. All animals, except one, were hypertensive during anesthesia. Heart rate during anesthesia was significantly increased, compared with control measurements, and cardiac output was decreased. Plasma glucose and lactate values significantly increased when the animals were restrained on their sides. Plasma glucose concentrations remained increased during anesthesia, but lactate decreased. Packed cell volume and plasma proteins were unchanged by the induction of anesthesia. Plasma norepinephrine concentration was unchanged during anesthesia, and epinephrine concentration was decreased. Endotracheal intubation caused a transient significant increase in arterial pressure, heart rate, and thromboxane B2 and a nonsignificant increase in norepinephrine.

Topics: Anesthesia, General; Animals; Blood Glucose; Blood Pressure; Blood Proteins; Cattle; Epinephrine; Erythrocyte Volume; Guaifenesin; Halothane; Heart Rate; Hypertension; Lactates; Male; Norepinephrine; Orchiectomy; Thiobarbiturates; Thromboxane B2