2009
DOI: 10.1016/j.vph.2008.12.001
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Role of angiotensin II in the response to endothelin-1 of goat cerebral arteries after ischemia–reperfusion

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Cited by 5 publications
(7 citation statements)
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“…Ang II potentiates vasoconstriction to ET-1 in cerebral arteries after ischemia and reperfusion but not under non-ischemic control conditions. 115 Activation of ET-1 receptors during ischemia and reperfusion has been shown to produce reactive oxygen (ROS) and nitrogen (RONS) species in an endothelium-dependent manner, that may be enhanced during hypertension in which ET-1 is elevated. 116 A previous study found that brain parenchymal arterioles (PAs) constricted to sarafotoxin, a selective ET B receptor agonist, only after tMCAO that was prevented by FeTMPyP to scavenge ONOO À , suggesting that ET-1 activation of ET B receptors on endothelium produces ONOO À to cause vasoconstriction.…”
Section: Endothelinmentioning
confidence: 99%
See 1 more Smart Citation
“…Ang II potentiates vasoconstriction to ET-1 in cerebral arteries after ischemia and reperfusion but not under non-ischemic control conditions. 115 Activation of ET-1 receptors during ischemia and reperfusion has been shown to produce reactive oxygen (ROS) and nitrogen (RONS) species in an endothelium-dependent manner, that may be enhanced during hypertension in which ET-1 is elevated. 116 A previous study found that brain parenchymal arterioles (PAs) constricted to sarafotoxin, a selective ET B receptor agonist, only after tMCAO that was prevented by FeTMPyP to scavenge ONOO À , suggesting that ET-1 activation of ET B receptors on endothelium produces ONOO À to cause vasoconstriction.…”
Section: Endothelinmentioning
confidence: 99%
“…Ang II potentiates vasoconstriction to ET-1 in cerebral arteries after ischemia and reperfusion but not under non-ischemic control conditions. 115…”
Section: Vasoconstrictor Stimuli During Hypertensionmentioning
confidence: 99%
“…Thus, inhibition of A‐II synthesis might have a protective effect on IR injury. Several studies have reported that selective ARB and ACE inhibitors might reduce various IR‐induced tissue damage, such as myocardial, hepatic, renal, cerebral and intestinal 12–17 . The effects of these drugs were also investigated by Gokce et al .…”
Section: Introductionmentioning
confidence: 99%
“…Several studies have reported that selective ARB and ACE inhibitors might reduce various IR-induced tissue damage, such as myocardial, hepatic, renal, cerebral and intestinal. [12][13][14][15][16][17] The effects of these drugs were also investigated by Gokce et al in a testicular IR model. They reported that administration of lisinopril, an ACE inhibitor, and losartan, an ARB, decreased the histopathological injury and apoptosis in the contralateral testes (non-ischemic), but they did not present the results of ipsilateral testes (ischemic).…”
Section: Introductionmentioning
confidence: 99%
“…vasoconstriction and hypoperfusion) [ 61 , 62 , 63 , 64 , 65 , 66 , 67 , 68 ]. The molecular mechanism underlying these effects was attributed mainly to the activation of angiotensin II (ANG II) and the subsequent increase in the production of reactive oxygen species (ROS) and the activation of phospholipase C (PLC) [ 67 , 69 , 70 , 71 , 72 , 73 , 74 ]. Each of these pathways may activate a particular mechanism to increase the risk of stroke.…”
Section: Resultsmentioning
confidence: 99%