Dual role of nitric oxide in gastric hypersecretion in the distended stomach: Inhibition of acid secretion and stimulation of pepsinongen secretion

Life Sciences ◽  
2008 ◽  
Vol 83 (25-26) ◽  
pp. 886-892 ◽  
Author(s):  
Yasuyuki Ito ◽  
Sayaka Okuda ◽  
Fumikazu Ohkawa ◽  
Shinichi Kato ◽  
Shoji Mitsufuji ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Acid Secretion ◽  
Dual Role ◽  
Gastric Hypersecretion ◽  
Distended Stomach ◽  
Stimulation Of

Role of nitric oxide in gastric hyperemia induced by central vagal stimulation

1993 ◽  
Vol 264 (2) ◽  
pp. G280-G284 ◽  
Author(s):  
T. Tanaka ◽  
P. Guth ◽  
Y. Tache
Keyword(s):  
Nitric Oxide ◽  
Acid Secretion ◽  
Vagal Stimulation ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Hydrogen Gas ◽  
Hydrogen Gas Clearance ◽  
Intracisternal Injection ◽  
Stimulation Of

The effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, on the vagal cholinergic increase in gastric mucosal blood flow (GMBF) and acid secretion induced by intracisternal injection of the thyrotropin-releasing hormone (TRH) analogue, RX 77368, were studied. GMBF and acid secretion were measured simultaneously by the hydrogen gas clearance technique and titration of gastric perfusate in urethan-anesthetized rats. RX 77368 (30 ng) injected intracisternally stimulated gastric acid secretion and GMBF for 90 and 180 min respectively. GMBF was increased from basal 63 +/- 4 to 166 +/- 14 ml.min-1.100 g-1 at 60 min postinjection. L-NAME (3 mg/kg) injected intravenously 15 min before RX 77368 completely prevented the increase in GMBF induced by the TRH analogue, whereas the acid response was not modified. The effect of L-NAME was reversed by L-arginine but not by the stereoisomer D-arginine. These results show that the increase in GMBF, but not the stimulation of acid secretion, induced by central vagal activation is mediated through a product of L-arginine-NO pathway.

Dual Role of Nitric Oxide in the Pathogenesis of Parkinson's Disease

2014 ◽  
Vol 1 (4) ◽  
pp. 243-253 ◽  
Author(s):  
Vaibhav Walia ◽  
Anuradha Sharma ◽  
Monika Gahlawat ◽  
O. P. Dube
Keyword(s):  
Nitric Oxide ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Dual Role

Dual Role of Nitric Oxide in Cancer Biology

2010 ◽  
pp. 39-57 ◽  
Author(s):  
Shehla Pervin ◽  
Rajan Singh ◽  
Suvajit Sen ◽  
Gautam Chaudhuri
Keyword(s):  
Nitric Oxide ◽  
Cancer Biology ◽  
Dual Role

Role of AT1 receptors in the renal papillary effects of acute and chronic nitric oxide inhibition

1998 ◽  
Vol 274 (3) ◽  
pp. R760-R766 ◽  
Author(s):  
M. Clara Ortíz ◽  
Lourdes A. Fortepiani ◽  
Francisco M. Ruiz-Marcos ◽  
Noemí M. Atucha ◽  
Joaquín García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Chronic Administration ◽  
Acute Administration ◽  
Synthesis Inhibitor ◽  
Renal Vasoconstriction ◽  
Oxide Inhibition ◽  
Stimulation Of

Nitric oxide (NO) is a vasodilator substance controlling renal papillary blood flow (PBF) in the rat. In this study we have evaluated the role of AT1 angiotensin II receptors as modulators of the whole kidney and papillary vasoconstrictor effects induced by the acute or chronic inhibition of NO synthesis. Experiments have been performed in anesthetized, euvolemic Munich-Wistar rats prepared for the study of renal blood flow (RBF) and PBF. In normal rats, acute administration of the NO synthesis inhibitor N ω-nitro-l-arginine methyl ester (l-NAME) increased mean arterial pressure (MAP) and decreased RBF and PBF. Either acute or chronic treatment with the AT1 receptor blocker losartan did not modify the decreases in RBF or PBF secondary to l-NAME. In animals made hypertensive by chronic inhibition of NO, basal MAP was higher, whereas RBF and PBF were lower than in the controls. In these animals, acute or chronic administration of losartan decreased MAP and increased both RBF and PBF significantly. These results indicate that, under normal conditions, the decreases in RBF or PBF induced by the acute inhibition of NO synthesis are not modulated by AT1-receptor stimulation. However, the arterial hypertension, renal vasoconstriction, and reduced PBF present in chronic NO-deficient hypertensive rats is partially due to the effects of angiotensin II, via stimulation of AT1-receptors.

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