Naslov
Role of arachidonic acid metabolites in the dysregulation of cerebral circulation

Autori
Drenjančević, Ines

Vrsta, podvrsta i kategorija rada
Sažeci sa skupova, sažetak, znanstveni

Izvornik
A Magyar Hypertonia Tarsasag. XI. Nemzetkozi Tovabbkepzo Eloadas-sorozata es XX KOngresszusa : u: Hypertonia es nephrologia 16 (2012) (S3) / - Budimpešta, 2012, 50-50

Skup
A Magyar Hypertonia Tarsasag. XI. Nemzetkozi Tovabbkepzo Eloadas-sorozata es XX KOngresszusa

Mjesto i datum
Budimpešta, Mađarska, 09.12.2012. - 12.12.2012

Vrsta sudjelovanja
Pozvano predavanje

Vrsta recenzije
Međunarodna recenzija

Ključne riječi
arachidonic acid; 20-HETE; EETs; cerebral blood flow

Sažetak
Maintenance of appropriate cerebral blood flow (CBF) is necessary for overall adequate oxygenation of the brain as well as to increase blood flow to areas of the brain with increased neuronal activity, simultaneously preserving the intracranial volume and pressure in physiological range. CBF is autoregulated over a wide range of arterial pressures via local myogenic, metabolic and flow- mediated regulatory mechanisms (1, 2). Several endothelium-derived factors were shown to mediate the regulation of CBF, among which the metabolites of arachidonic acid (AA) have very important role. AA could be metabolized via three pathways- via cyclooxygenases (COX) to prostaglandins and thromboxanes, via lypooxygenase to leukotrienes and via P450 (CYP) pathway to epoxyeicosatrienoic acids (EETs) and 20-hydroxyeicosatetraenoic acid (20-HETE). All of them could contribute to dysregulation of the cerebral blood flow in condition such as hypertension, diabetes mellitus or ischemic stroke. Lately, particular attention is paid to CYP450 metabolites since many experimental studies have shown that 20-hydroxyeicosatetraenoic acid (20-HETE) is a powerful constrictor of cerebral vessels, and a key mediator of the myogenic response and autoregulation of cerebral blood flow, but also mediates vasoconstriction of cerebral resistance vessels in response to increase in flow (2). 20-HETE contributes to oxidative stress, endothelial dysfunction, and the enhanced sensitivity to ischemic stroke (3). On the other hand, EETs have been demonstrated to be key mediators coupling neuronal activity and astrocytes to evoke cerebral arteriolar dilatory responses (1). Inhibition of 20-HETE and/or increasing of EETs levels may decrease cerebral blood flow impairment and cerebral

Izvorni jezik
Engleski

Znanstvena područja
Temeljne medicinske znanosti, Kliničke medicinske znanosti

POVEZANOST RADA