scholarly journals Blood pressure response to hypoxia: role of nitric oxide synthase

2003 ◽  
Vol 16 (12) ◽  
pp. 1043-1048 ◽  
Author(s):  
C Barton
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Oxide Synthase

scholarly journals Effect of an Inhibitor of Neuronal Nitric Oxide Synthase 7-Nitroindazole on Cerebral Hemodynamic Response and Brain Excitability in Urethane-Anesthetized Rats

2013 ◽  
pp. S57-S66 ◽  
Author(s):  
C. BROŽÍČKOVÁ ◽  
J. OTÁHAL
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Neurovascular Coupling ◽  
Neuronal Nitric Oxide Synthase ◽  
Hemodynamic Response ◽  
Doppler Flowmetry ◽  
Arterial Blood ◽  
Oxide Synthase

The role of neuronal nitric oxide synthase (nNOS) in the pathophysiology of epilepsy and seizures remains disputable. One of the reasons why results from the acute in vivo studies display controversies might be the effect on the regulation of cerebral blood flow (CBF) during pharmacologically induced alterations of NO system. We examined neurovascular coupling in the rat sensorimotor cortex in response to transcallosal stimulation under nNOS inhibition by 7-nitroindazole (7-NI). Adult Wistar rats were anesthetized with urethane and epidural silver EEG electrodes were implanted over sensorimotor cortices. Regional CBF was measured by Laser Doppler Flowmetry (LDF). We catheterized a common carotid artery to measure arterial blood pressure (BP). 7-NI did not significantly affect blood pressure and heart rate. Electrophysiological recordings of evoked potentials (EPs) revealed no effect on their amplitude, rhythmic potentiation or depression of EPs. Transcallosal stimulation of the contralateral cortex induced a frequency dependent rise in CBF. Although 7-NI did not significantly affect basal CBF and cortical excitability, hemodynamic responses to the transcallosal stimulation were diminished implicating a role of nNOS in neurovascular coupling. Urethane anesthesia is suitable for future epileptological experiments. Our findings demonstrate that NO contributes to the hemodynamic response during brain activation.

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