2005
DOI: 10.1016/j.phrs.2005.04.001
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Inhibition of Ca/calmodulin-dependent protein kinase II, RAS-GTPase and 20-hydroxyeicosatetraenoic acid attenuates the development of diabetes-induced vascular dysfunction in the rat carotid artery

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Cited by 32 publications
(21 citation statements)
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“…POE attenuated the increased contractile responses to both agonists with an accompanying reduction in sensitivity (Tables 7 and 8). It has been previously suggested that impaired NO synthesis may contribute to exaggerated effects of vasoconstrictors in diabetic animals (Benter et al, 2005). In our study, treatment with LNA did not further augment the PE and 5-HT contractions in diabetic aortic rings (data not shown), ruling out the possibility that impaired NO synthesis may interfere with increased contractile responses.…”
Section: Discussionsupporting
confidence: 44%
“…POE attenuated the increased contractile responses to both agonists with an accompanying reduction in sensitivity (Tables 7 and 8). It has been previously suggested that impaired NO synthesis may contribute to exaggerated effects of vasoconstrictors in diabetic animals (Benter et al, 2005). In our study, treatment with LNA did not further augment the PE and 5-HT contractions in diabetic aortic rings (data not shown), ruling out the possibility that impaired NO synthesis may interfere with increased contractile responses.…”
Section: Discussionsupporting
confidence: 44%
“…Impaired NO synthesis is known to increase vasocontractility in diabetic animals (Benter et al, 2005). However, in our study, inhibition of NO synthesis by L-NAME did not result in further increments in phenylephrine and 5-HT contractions.…”
Section: Discussioncontrasting
confidence: 75%
“…It has recently been suggested that activation of a mitochondrial/ox-CaMKII pathway contributes to increased sudden death in diabetic patients after myocardial infarction (Luo et al, 2013). CaMKII pathway has been implicated in diabetic retinopathy development, diabetic vascular dysfunction and renal dysfunction in a model of insulin-dependent diabetes (Benter et al, 2005;Kato et al, 2008;Kim et al, 2010). Our results are the first report indicating that CaMKII pathway should be further explored in the context of diabetic complications.…”
Section: Discussionsupporting
confidence: 52%