The role of oxidant stress in angiotensin II-mediated contraction of human resistance arteries in the state of health and the presence of cardiovascular disease.

BACKGROUND: Angiotensin II is a powerful vasoconstrictor and regulator of cardiovascular growth. Also, it increases formation of reactive oxygen species and contributes to vascular dysfunction. We investigated the role of oxidant stress in contraction of human resistance arteries to angiotensin II, in health and in the presence of cardiovascular disease. METHODS AND PATIENTS: Studies of isometric contraction to angiotensin II, using human resistance arteries from healthy volunteers and patients, undergoing cardiac revascularization surgery, were performed by the broad-spectrum antioxidant agent vitamin C and superoxide dismutase mimetic TEMPOL. In the presence of vitamin C, the potency and the maximum contractile response were reduced in both patients and healthy volunteers. Addition of TEMPOL caused a decrease in angiotensin II-induced contraction only in the patients' group. CONCLUSIONS: Our studies provide evidence for the role of oxidant stress in the contractile response of human resistance arteries to angiotensin II. In patients with cardiovascular disease, the superoxide anion may be the major species involved. In healthy subjects, other reactive oxygen species and the redox-independent vasoconstrictor action of angiotensin II predominate. CONDENSED ABSTRACT: Increased formation of reactive oxygen species, due to angiotensin II, contributes to vascular dysfunction. We determined the oxidative reactivity of human resistance arteries to angiotensin II in healthy subjects and patients, undergoing cardiac revascularization surgery, using the broad-spectrum antioxidant agent, vitamin C, and superoxide dismutase mimetic, TEMPOL. There was a large decrease in potency and maximum of angiotensin II-induced contractile response noted in both groups with the former, while the latter reduced contraction only in the patients' group. Superoxide anion may play a major role in angiotensin II contractions of human resistance arteries in the presence of cardiovascular disease. In healthy subjects, other reactive species and the redox-independent pathways predominate.

Role of oxidative stress in angiotensin-II mediated contraction of human conduit arteries in patients with cardiovascular disease.

BACKGROUND: Angiotensin II is a powerful vasoconstrictor involved in the development of high blood pressure and in the regulation of cardiovascular growth. Recent reports have suggested that in addition to the classical pathways involved in transducing responses to receptor activation, formation of reactive oxygen species by angiotensin II may also be involved. We investigated the importance of oxidative stress in angiotensin II induced contraction in human conduit arteries from patients with cardiovascular disease. METHODS AND RESULTS: Isometric contraction studies using human radial arteries entailed probes modulating the redox-dependent reactions to define the oxidative pathways involved in angiotensin II contraction. In situ oxidative fluorescence was employed to detect immediate superoxide tissue production in radial and internal mammary arteries. Treatment with TEMPOL, human superoxide dismutase, diphenyleneiodonium, oxypurinol, NG-monomethyl L-arginine considerably decreased contractile response to angiotensin II in radial arteries. Similarly, angiotensin II-stimulated arterial superoxide production was reduced in the presence of the above inhibitors. On the contrary, used as controls, norepinephrine vasoconstriction was not associated with increase of superoxide and neither ciprofloxacin nor aminophylline altered basal or angiotensin II induced superoxide generation. CONCLUSIONS: Our findings provide evidence for the role of oxidative pathways in contractile response of human conduit arteries to angiotensin II. Angiotensin II induced superoxide anion production may be mediated by multiple inter-dependent rate-limiting enzymes in both types of artery. Our studies may have important implication for future therapeutic approaches involving inhibition of angiotensin II mediated superoxide generation in hypertension and prevention of cardiovascular disease. CONDENSED ABSTRACT: We studied the role of oxidant species in contraction responses to angiotensin II in human conduit arteries. Treating radial artery segments with the anti-oxidants with a range of inhibitors, affecting the redox dependent pathways, markedly reduced contraction to angiotensin II. In parallel experiments, oxidative fluorescence was assessed and compared in human radial and internal mammary artery. Angiotensin II induced superoxide anion production may be mediated by multiple inter-dependent rate-limiting enzymes in both types of artery.

137Cs-uptake into wheat (Triticum vulgare) plants from five representative soils of Bangladesh.

A pot experiment was conducted to study the uptake of 137Cs by wheat grown in five representative soils of Bangladesh having different soil characteristics. Artificial application of 137Cs increased the activity in soils up to 45.9 Bq/kg soil, measured at the end of the harvest of wheat crop. Different plant parts had different ability to accumulate 137Cs. Grains had the least activity and transfer factor, while the highest activity and lowest transfer factor were measured in roots, which restricted translocation of 137Cs to wheat straw. The result showed that the transfer factors (mean value) varied from 0.05 to 0.114 in wheat straw, 0.066-0.133 in roots and 0.011-0.043 in wheat grains. The activity and transfer factor of radioactive cesium in wheat plants were found to be greatly influenced by soil properties, i.e. clay content, K, organic matter, CEC, pH, exchangeable ions, etc. Cation exchange capacity and calcium in soils influenced positively, while clay minerals, exchangeable K and organic matter, negatively affected the 137Cs activity concentrations in wheat plants.

Abnormal vasoconstrictor responses to angiotensin II and noradrenaline in isolated small arteries from patients with cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL).

BACKGROUND AND PURPOSE: Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is characterized by ultrastructural abnormalities in small cerebral and systemic vessels. We assessed vasomotor function in systemic small arteries in CADASIL. METHODS: We studied 10 CADASIL patients and 10 control subjects. Resistance arteries isolated from gluteal biopsies were mounted on small-vessel myographs, and concentration responses were determined for vasoconstrictors (noradrenaline, angiotensin II, and endothelin-I) and vasodilators (acetylcholine, bradykinin, spermine-NONOate, and nifedipine). Maximum data are shown as percent potassium contraction. RESULTS: There was reduced potency for noradrenaline in CADASIL (CADASIL [38 arteries]: EC50, 240 nmol/L; control subjects [27 arteries]: EC50, 100 nmol/L; 2-way analysis of variance, F=9.76, P=0.002). Maximum response to angiotensin II was greater in CADASIL (120+/-8% versus 97+/-5% in control subjects; F=4.28, P=0.043). Tachyphylaxis to angiotensin II occurred in all control subjects studied but in only 3 of 9 CADASIL subjects (P=0.011, Fisher's exact test). Vasodilation was similar in CADASIL patients compared with control subjects for endothelium-dependent dilators (acetylcholine and bradykinin) and endothelium-independent dilators (spermine-NONOate and nifedipine). CONCLUSIONS: These results suggest a selective systemic microvascular vasoconstrictor abnormality in CADASIL in noradrenaline and angiotensin II pathways that is not explained by vasodilator impairment in endothelium or vascular smooth muscle. This could have important implications for prophylaxis and treatment of CADASIL.