scholarly journals Low [NaCl]-induced neuronal nitric oxide synthase (nNOS) expression and NO generation are regulated by intracellular pH in a mouse macula densa cell line (NE-MD)

2009 ◽  
Vol 59 (3) ◽  
pp. 165-173 ◽  
Author(s):  
Hideaki Kawada ◽  
Yukiko Yasuoka ◽  
Hidekazu Fukuda ◽  
Katsumasa Kawahara
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cell Line ◽  
Intracellular Ph ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Oxide Synthase ◽  
Nnos Expression

scholarly journals Anteroventral third ventricle (AV3V) lesion affects hypothalamic neuronal nitric oxide synthase (nNOS) expression following water deprivation

2011 ◽  
Vol 86 (3-4) ◽  
pp. 239-245 ◽  
Author(s):  
Fábio Alves Aguila ◽  
Gabriela Ravanelli Oliveira-Pelegrin ◽  
Song Tieng Yao ◽  
David Murphy ◽  
Maria José Alves Rocha
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Water Deprivation ◽  
Third Ventricle ◽  
Neuronal Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Nnos Expression

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 Optogenetic Stimulation Reduces Neuronal Nitric Oxide Synthase Expression After Stroke

Neurosurgery ◽  
2019 ◽  
Vol 66 (Supplement_1) ◽  
Author(s):  
Arjun Vivek Pendharkar ◽  
Daniel L Smerin ◽  
Lorenzo Gonzales ◽  
Eric Wang ◽  
Sabrina L Levy ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Motor Cortex ◽  
Functional Recovery ◽  
Neuronal Nitric Oxide Synthase ◽  
Optogenetic Stimulation ◽  
Oxide Synthase ◽  
Nnos Expression ◽  
Stimulation Of ◽  
Nnos Inhibition

Abstract INTRODUCTION Poststroke optogenetic stimulation has been shown to enhance neurovascular coupling and functional recovery. Neuronal nitric oxide synthase (nNOS) has been implicated as a key regulator of neurovascular response in acute stroke but its role in subacute recovery remains unclear. Here we investigate nNOS expression in stroke mice undergoing optogenetic stimulation of the contralesional lateral cerebellar nucleus (cLCN). We also examine the effects of nNOS inhibition on functional recovery using a pharmacological inhibitor targeting nNOS. METHODS Transgenic Thy1-ChR2-YFP male mice (10-12 wk) were used. Stereotaxic surgery was performed to implant a fiber cannula in the cLCN and animals underwent intraluminal middle cerebral artery suture occlusion (30 min). Optogenetic stimulation began at poststroke (PD) day 5 and continued until PD14. Sensorimotor tests were used to assess behavioral recovery at PD4, 7, 10, and 14. At PD15, primary motor cortex from both ipsi- and contralesional motor cortex (iM1, cM1) were dissected. nNOS mRNA and protein levels were examined using quantitative polymerase chain reaction and western blot. In another set of studies, nNOS inhibitor ARL 17477 dihydrochloride (10 mg/kg, intraperitoneally) was administered daily between PD5-14 and functional recovery was evaluated using sensorimotor tests. RESULTS cLCN stimulated stroke mice demonstrated significant improvement in speed (cm/s) on the rotating beam task at PD10 and 14 day (P < .05, P < .001 respectively). nNOS mRNA and protein expression was significantly and selectively decreased in cM1 of cLCN stimulated mice (P < .05). The reduced nNOS expression in cM1 was negatively correlated with improved recovery (R2 = −0.839, Pearson P = .009). nNOS inhibitor-treated stroke mice exhibited a significant functional improvement in speed at PD10, when compared to stroke mice receiving vehicle (saline) (P < .05). CONCLUSION Our results suggest that nNOS may play a maladaptive role in poststroke recovery. Optogenetic stimulation of cLCN and systemic nNOS inhibition produce functional benefits after stroke.

Region-specific alterations of neuronal nitric oxide synthase (nNOS) expression in the amygdala of the aged rats

2004 ◽  
Vol 999 (2) ◽  
pp. 231-236 ◽  
Author(s):  
Kyeung Min Joo ◽  
Yoon Hee Chung ◽  
Chung Min Shin ◽  
Yun Jung Lee ◽  
Choong Ik Cha
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Neuronal Nitric Oxide Synthase ◽  
Aged Rats ◽  
Oxide Synthase ◽  
Nnos Expression

Neuronal Nitric Oxide Synthase-Mediated Genotoxicity of 2-Methoxyestradiol in Hippocampal HT22 Cell Line

2015 ◽  
Vol 53 (7) ◽  
pp. 5030-5040 ◽  
Author(s):  
Magdalena Gorska ◽  
Michal A. Zmijewski ◽  
Alicja Kuban-Jankowska ◽  
Maciej Wnuk ◽  
Iwona Rzeszutek ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Cell Line ◽  
Neuronal Nitric Oxide Synthase ◽  
Ht22 Cell ◽  
Oxide Synthase

scholarly journals Lack of contribution of nitric oxide synthase to cholinergic vasodilation in murine renal afferent arterioles

2018 ◽  
Vol 314 (6) ◽  
pp. F1197-F1204 ◽  
Author(s):  
Sungmi Park ◽  
Benjamin J. Bivona ◽  
Lisa M. Harrison-Bernard
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Knockout Mice ◽  
Neuronal Nitric Oxide Synthase ◽  
Macula Densa ◽  
Afferent Arteriole ◽  
Wild Type ◽  
Afferent Arterioles ◽  
Nos Inhibitor ◽  
Oxide Synthase

We have previously reported significant increases in neuronal nitric oxide synthase (NOS) immunostaining in renal arterioles of angiotensin type 1A receptor (AT1A) knockout mice, and in arterioles and macula densa cells of AT1A/AT1B knockout mice. The contribution of nitric oxide derived from endothelial and macula densa cells in the maintenance of afferent arteriolar tone and acetylcholine-induced vasodilation was functionally determined in kidneys of wild-type, AT1A, and AT1A/AT1B knockout mice. Acetylcholine-induced changes in arteriolar diameters of in vitro blood-perfused juxtamedullary nephrons were measured during control conditions, in the presence of the nonspecific NOS inhibitor, Nω-nitro-l-arginine methyl ester (NLA), or the highly selective neuronal NOS inhibitor, N5-(1-imino-3-butenyl)-l-ornithine (VNIO). Acetylcholine (0.1 mM) produced a significant vasoconstriction in afferent arterioles of AT1A/AT1B mice (−10.9 ± 5.1%) and no changes in afferent arteriolar diameters of AT1A knockout mice. NLA (0.01–1 mM) or VNIO (0.01–1 μM) induced significant dose-dependent vasoconstrictions (−19.8 ± 4.0% 1 mM NLA; −7.8 ± 3.5% 1 μM VNIO) in afferent arterioles of kidneys of wild-type mice. VNIO had no effect on afferent arteriole diameters of AT1A knockout or AT1A/AT1B knockout mice, suggesting nonfunctional neuronal nitric oxide synthase. These data indicate that acetylcholine produces a significant renal afferent arteriole vasodilation independently of nitric oxide synthases in wild-type mice. AT1A receptors are essential for the manifestation of renal afferent arteriole responses to neuronal nitric oxide synthase-mediated nitric oxide release.

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