Role of macula densa neuronal nitric oxide synthase in renal diseases

2006 ◽  
Vol 39 (1) ◽  
pp. 2-7 ◽  
Author(s):  
Akihiro Tojo ◽  
Maristela Lika Onozato ◽  
Toshiro Fujita
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Renal Diseases ◽  
Oxide Synthase

scholarly journals Role of neuronal nitric oxide synthase in the macula densa

2001 ◽  
Vol 60 (5) ◽  
pp. 1676-1683 ◽  
Author(s):  
Yilin Ren ◽  
Jeffrey L. Garvin ◽  
Sadayoshi Ito ◽  
Oscar A. Carretero
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Oxide Synthase

Role of neuronal nitric oxide synthase (nNOS) in Duchenne and Becker muscular dystrophies – Still a possible treatment modality?

2018 ◽  
Vol 28 (11) ◽  
pp. 914-926 ◽  
Author(s):  
Nanna W. Dombernowsky ◽  
Joakim N.E. Ölmestig ◽  
Nanna Witting ◽  
Christina Kruuse
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Treatment Modality ◽  
Neuronal Nitric Oxide Synthase ◽  
Muscular Dystrophies ◽  
Oxide Synthase

scholarly journals The Role of Neuronal Nitric Oxide Synthase in Regulation of Cerebral Blood Flow in Normocapnia and Hypercapnia in Rats

1995 ◽  
Vol 15 (5) ◽  
pp. 774-778 ◽  
Author(s):  
Qiong Wang ◽  
Dale A. Pelligrino ◽  
Verna L. Baughman ◽  
Heidi M. Koenig ◽  
Ronald F. Albrecht
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Nitric Oxide Synthase ◽  
Inhibitory Action ◽  
Neuronal Nitric Oxide Synthase ◽  
Muscarinic Agonist ◽  
Doppler Flowmetry ◽  
Nos Inhibitors ◽  
Oxide Synthase

The nitric oxide synthase (NOS) inhibitors, nitro-L-arginine, its methyl ester, and N-monomethyl-L-arginine, have been shown to attenuate resting CBF and hypercapnia-induced cerebrovasodilation. Those agents nonspecifically inhibit the endothelial and neuronal NOS (eNOS and nNOS). 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. CBF was monitored using laser-Doppler flowmetry. Administration of 7-NI (80 mg kg−1 i.p.) reduced cortical brain NOS activity by 57%, the resting CBF by 19–27%, and the CBF response to hypercapnia by 60%. The 60% reduction was similar in magnitude to the CBF reductions observed in previous studies in which nonspecific NOS inhibitors were used. In the present study, 7-NI did not increase the MABP. Furthermore, the CBF response to oxotremorine, a blood–brain barrier permeant muscarinic agonist that induces cerebrovasodilation via endothelium-derived NO, was unaffected by 7-NI. These results confirmed that 7-NI does not influence eNOS; they also indicated that the effects of 7-NI on the resting CBF and on the CBF response to hypercapnia in this study were solely related to its inhibitory action on nNOS. The results further suggest that the NO synthesized by the action of nNOS participates in regulation of basal CBF and is the major, if not the only, category of NO contributing to the hypercapnic CBF response.

Neuronal nitric oxide synthase modulates rat renal microvascular function

1998 ◽  
Vol 274 (3) ◽  
pp. F516-F524 ◽  
Author(s):  
Atsuhiro Ichihara ◽  
Edward W. Inscho ◽  
John D. Imig ◽  
L. Gabriel Navar
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Vasoconstrictor Response ◽  
Arteriolar Tone ◽  
Oxide Synthase

This study was performed to determine the influence of neuronal nitric oxide synthase (nNOS) on renal arteriolar tone under conditions of normal, interrupted, and increased volume delivery to the macula densa segment and on the microvascular responses to angiotensin II (ANG II). Experiments were performed in vitro on afferent (21.2 ± 0.2 μm) and efferent (18.5 ± 0.2 μm) arterioles of kidneys harvested from male Sprague-Dawley rats, using the blood-perfused juxtamedullary nephron technique. Superfusion with the specific nNOS inhibitor, S-methyl-l-thiocitrulline (l-SMTC), decreased afferent and efferent arteriolar diameters, and these decreases in arteriolar diameters were prevented by interruption of distal volume delivery by papillectomy. When 10 mM acetazolamide was added to the blood perfusate to increase volume delivery to the macula densa segment, afferent arteriolar vasoconstrictor responses tol-SMTC were enhanced, but this effect was again completely prevented after papillectomy. In contrast, the arteriolar diameter responses to the nonselective NOS inhibitor, N ω-nitro-l-arginine (l-NNA) were only attenuated by papillectomy.l-SMTC (10 μM) enhanced the efferent arteriolar vasoconstrictor response to ANG II but did not alter the afferent arteriolar vasoconstrictor responsiveness to ANG II. In contrast, l-NNA (100 μM) enhanced both afferent and efferent arteriolar vasoconstrictor responses to ANG II. These results indicate that the modulating influence of nNOS on afferent arteriolar tone of juxtamedullary nephrons is dependent on distal tubular fluid flow. Furthermore, nNOS exerts a differential modulatory action on the juxtamedullary microvasculature by enhancing efferent, but not afferent, arteriolar responsiveness to ANG II.

scholarly journals Regulation of myocyte contraction via neuronal nitric oxide synthase: role of ryanodine receptorS-nitrosylation

2010 ◽  
Vol 588 (15) ◽  
pp. 2905-2917 ◽  
Author(s):  
Honglan Wang ◽  
Serge Viatchenko-Karpinski ◽  
Junhui Sun ◽  
Inna Györke ◽  
Nancy A. Benkusky ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ryanodine Receptors ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase
Sign in / Sign up

Export Citation Format

Share Document