Avtor/Urednik     Puentmann, Valentina
Naslov     Prispevek reaktivnih kisikovih spojin h kontrakciji človeških prevodnih arterij pod vplivom angiotenzina II
Prevedeni naslov     Contribution of reactive oxygen species to angiotensin II induced contraction of human conduit arteries
Tip     monografija
Kraj izdaje     Ljubljana
Založnik     Medicinska fakulteta
Leto izdaje     2003
Obseg     str. 69
Jezik     slo, eng
Abstrakt     An increasing body of evidence implicates oxidant stress in the pathogenesis of many cardiovascular diseases, with induction of endothelial dysfunction as a possible mechanism in common. Angiotensin II (Ang-II) classically causes vascular contraction via the AT1-receptor and phospholipase C transducing intracellular mechanisms that involve protein kinase C (PKC). It has also recently been reported that Ang-II increases superoxide anion production in human arteries by an AT1-dependent mechanism via activating NAD(P)H oxidase. In animal models, xanthine oxidase and endothelial nitric oxide synthase (eNOS) have been also implicated. Whether oxidant stress plays a significant role in Ang-II -induced vascular contraction in human conduit arteries and what are the underlying biochemical pathways remains unclear. Using classical organ bath pharmacology, concentration response curves were obtained to Ang-II in segments of radial artery (RA) from patients undergoing routine coronary revascularization. Probes that modulate reactions generating reactive oxygen species were used to identify the oxidant pathways and reactive oxidant species involved. In parallel experiments, oxidative fluorescence was assessed and compared in human RA and internal mammary artery (IMA). The semi-quantitative digital microscopy was used to evaluate changes in situ concentration of superoxide anion in response to Ang-II. In organ bath studies, in the presence of the superoxide scavenger TEMPOL or superoxide dismutase (SOD), pEC50 was little different but the maximum contractile response to Ang-II was significantly reduced (control vs. TEMPOL: pEC50 9.4 +- 0.2 (SE) vs. 9.3 +- 0.1, maximum response 95 +- 8% vs. 65 +- 5%, n = 10, 2-way ANOVA F = 31.1, p < 0.0001; control vs. SOD: pEC50 9.1 +- 0.1 vs. 9.3 +- 0.3, maximal response 85 +- 6% vs. 64 +- 7%, 2-way ANOVA F=41.3, p < 0.0001). (Abstract truncated at 2000 characters).
Deskriptorji     RADIAL ARTERY
MAMMARY ARTERIES
ENDOTHELIUM, VASCULAR
VASOCONSTRICTION
ANGIOTENSIN II
REACTIVE OXYGEN SPECIES
OXIDATIVE STRESS
DOSE-RESPONSE RELATIONSHIP, DRUG
MICROSCOPY, FLUORESCENCE
SUPEROXIDES
SUPEROXIDE DISMUTASE
OXYPURINOL
OMEGA-N-METHYLARGININE
ANALYSIS OF VARIANCE