Neuronal nitric oxide synthase contributes to the normalization of blood pressure in medicated hypertensive patients

Nitric Oxide ◽  
2018 ◽  
Vol 80 ◽  
pp. 98-107 ◽  
Author(s):  
Eduardo D. Costa ◽  
Josiane F. Silva ◽  
Rosária D. Aires ◽  
Daniela C. Garcia ◽  
Milhem J. Kansaon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypertensive Patients ◽  
Oxide Synthase

Chronic Blockade of Neuronal Nitric Oxide Synthase Does Not Affect Long-Term Control of Blood Pressure in Normal, Saline-Drinking or Deoxycorticosterone-Treated Rats

2003 ◽  
Vol 88 (2) ◽  
pp. 243-250 ◽  
Author(s):  
Rosemary Wangensteen ◽  
Juan Sainz ◽  
Isabel Rodríguez-Gomez ◽  
Juan Manuel Moreno ◽  
Antonio Osuna ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Normal Saline ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase

scholarly journals Neuronal nitric oxide synthase within paraventricular nucleus: blood pressure and baroreflex in two-kidney, one-clip hypertensive rats

2010 ◽  
Vol 95 (8) ◽  
pp. 845-857 ◽  
Author(s):  
Noreen F. Rossi ◽  
Maria Maliszewska-Scislo ◽  
Haiping Chen ◽  
Stephen M. Black ◽  
Shruti Sharma ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Paraventricular Nucleus ◽  
Neuronal Nitric Oxide Synthase ◽  
Hypertensive Rats ◽  
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.

scholarly journals Neuronal Nitric Oxide Synthase-Deficient Mice Have Impaired Renin Release But Normal Blood Pressure

2008 ◽  
Vol 21 (1) ◽  
pp. 111-116 ◽  
Author(s):  
J. Sallstrom ◽  
M. Carlstrom ◽  
B. L. Jensen ◽  
O. Skott ◽  
R. D. Brown ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Renin Release ◽  
Normal Blood ◽  
Normal Blood Pressure ◽  
Oxide Synthase ◽  
Deficient Mice

Defective fluid and HCO3 − absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice

2000 ◽  
Vol 279 (3) ◽  
pp. F518-F524 ◽  
Author(s):  
Tong Wang ◽  
Fiona M. Inglis ◽  
Robert G. Kalb
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Metabolic Acidosis ◽  
Nitric Oxide Synthase ◽  
Proximal Tubule ◽  
Knockout Mice ◽  
Neuronal Nitric Oxide Synthase ◽  
Fluid Absorption ◽  
Wild Type ◽  
Oxide Synthase

Using renal clearance techniques and in situ microperfusion of proximal tubules, we examined the effects of N G-monomethyl-l-arginine methyl ester (l-NAME) on fluid and HCO3 −transport in wild-type mice and also investigated proximal tubule transport in neuronal nitric oxide synthase (nNOS)-knockout mice. In wild-type mice, administration of l-NAME (3 mg/kg bolus iv) significantly increased mean blood pressure, urine volume, and urinary Na+ excretion. l-NAME, given by intravenous bolus and added to the luminal perfusion solution, decreased absorption of fluid (60%) and HCO3 − (49%) in the proximal tubule. In nNOS-knockout mice, the urinary excretion of HCO3 − was significantly higher than in the wild-type mice (3.12 ± 0.52 vs. 1.40 ± 0.33 mM) and the rates of HCO3 − and fluid absorption were 62 and 72% lower, respectively. Both arterial blood HCO3 − concentration (20.7 vs. 25.7 mM) and blood pH (7.27 vs. 7.34) were lower, indicating a significant metabolic acidosis in nNOS-knockout mice. Blood pressure was lower in nNOS-knockout mice (76.2 ± 4.6 mmHg) than in wild-type control animals (102.9 ± 8.4 mmHg); however, it increased in response to l-NAME (125.5 ± 5.07 mmHg). Plasma Na+ and K+ were not significantly different from control values. Our data show that a large component of HCO3 − and fluid absorption in the proximal tubule is controlled by nNOS. Mice without this isozyme are defective in absorption of fluid and HCO3 − in the proximal tubule and develop metabolic acidosis, suggesting that nNOS plays an important role in the regulation of acid-base balance.

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