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CEBPZ — NOS1

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Santizo et al., Neuroreport 2000 (Brain Ischemia) : In initial experiments, where ischemic MABP was targeted to exactly 30 mmHg, NOS inhibition reduced intra-ischemic cortical CBF from the control level of approximately 20 % of baseline to 3 % ( L-NNA ) or 6 % ( ARR 17477 ) of baseline
Larsen et al., J Hepatol 2001 (Brain Edema...) : The unique mechanism for the rise in CBF in hyperammonemia was not prevented by NOS inhibition indicating that NO is not the mediator of high CBF and intracranial hypertension
Zhiliaev et al., Ross Fiziol Zh Im I M Sechenova 2002 : Inhibition of NO--synthase type I and III (NOS) by L-NAME in the air caused the same decreasing of the CBF as at 4 ATA HBO
Wyatt et al., Am J Pathol 2003 : We have also shown that inhibitors of nitric oxide synthase block EtOH stimulated increases in CBF
Yusa et al., J Anesth 2000 : To evaluate factors involved in global forebrain ischemia-reperfusion, the effects of the systemically administered NOS inhibitor, N ( G ) -nitro-L-arginine methyl ester ( L-NAME ), on changes in extracellular glutamate and cerebral blood flow (CBF) were studied during the early period of global forebrain ischemia-reperfusion, simultaneously measuring the glutamate released in the rat forebrain cortex and cortical CBF
Hagioka et al., Neurosci Lett 2005 (Seizures) : To elucidate the origins of NO production during HBO ( 2 ) exposure, we examined the effects of the selective neuronal NO synthase (NOS) inhibitor, 7-nitroindazole ( 7-NI ), and the non-selective NOS inhibitor, N-nitro-l-arginine methyl ester ( l-NAME ), on changes in CBF and NO metabolites ( NO ( x ), nitrite and nitrate ) using a laser Doppler flow probe and in vivo microdialysis techniques, respectively
Wainwright et al., Neurosci Lett 2007 (Brain Injuries...) : We measured NO levels and CBF in the presence of either a NOS inhibitor, N-nitro-l-arginine methyl ester ( L-NAME ) or an NO donor ( Z ) -1- [ N- ( 2-amino-ethyl ) -N- ( 2-ammonio-ethyl ) amino ] diazen-1-ium-1,2-diolate ( DETANONOate )
Girouard et al., J Neurosci 2009 : We found that the CBF and ROS increases elicited by topical application of NMDA to the mouse neocortex were both dependent on neuronal NO synthase (nNOS) , cGMP, and the cGMP effector kinase protein kinase G ( PKG )
Shabeeh et al., Am J Physiol Heart Circ Physiol 2013 : Our results confirm a role of nNOS in the regulation of basal CBF in humans but show that coronary vasodilation in response to a pacing induced increase in cardiac workload is exclusively mediated by eNOS derived NO
Wang et al., J Cereb Blood Flow Metab 1995 (Hypercapnia) : In the present study, we used a novel nNOS inhibitor, 7-nitroindazole ( 7-NI ) to examine the role of nNOS in CBF during normocapnia and hypercapnia in fentanyl/N2O anesthetized rats
Jain et al., Biochem Biophys Res Commun 1993 : NOS inhibitor induced CBF slowing was also observed when cells were pre stimulated with either bradykinin or substance P and was completely reversed by L-arginine or SNP but not by D-arginine
Fabricius et al., Am J Physiol 1994 (Hypercapnia) : We examined the effect of nitric oxide synthase (NOS) inhibition and tetrodotoxin ( TTX ) on the increase of cerebral blood flow (CBF) in parietal ( CoBF ) and cerebellar cortex ( CeBF ) in response to hypercapnia
Pelligrino et al., Neuroreport 1998 (Brain Ischemia) : Intra-ischemic CBF was reduced by nNOS inhibition, with ARL 17477, in normal and low-dose E2-treated OVX rats ( 4-8 % baseline )