Vasoactive intestinal peptide and nitric oxide promote survival of adult rat myenteric neurons in culture

2003 ◽  
Vol 72 (5) ◽  
pp. 595-602 ◽  
Author(s):  
Katarina Sandgren ◽  
Zhong Lin ◽  
Åsa Fex Svenningsen ◽  
Eva Ekblad
Keyword(s):  
Nitric Oxide ◽  
Vasoactive Intestinal Peptide ◽  
Myenteric Neurons ◽  
Adult Rat

scholarly journals Vasoactive intestinal peptide stimulates mucus secretion, but nitric oxide has no effect on mucus secretion in the ferret trachea

2006 ◽  
Vol 101 (2) ◽  
pp. 486-491 ◽  
Author(s):  
Jung-Soo Kim ◽  
Kosuke Okamoto ◽  
Shinobu Arima ◽  
Bruce K. Rubin
Keyword(s):  
Nitric Oxide ◽  
Receptor Antagonist ◽  
Vasoactive Intestinal Peptide ◽  
Mucus Secretion ◽  
Cell Secretion ◽  
Mucin Secretion ◽  
No Donor ◽  
Peptide Analog ◽  
Dose Dependent ◽  
Vip Receptor

Vasoactive intestinal peptide (VIP) and nitric oxide (NO) are neurotransmitters involved in the regulation of bronchial and pulmonary vascular tone. Published studies of the effects of VIP on airway mucus secretion have yielded conflicting results. The purpose of this study was to determine the effect of VIP on mucus secretion in the ferret trachea and if this effect was influenced by NO. We used a sandwich enzyme-linked lectin assay to measure mucin secretion and a turbidimetric assay to measure lysozyme (serous cell) secretion from ferret tracheal segments. VIP (10−7 M) increased mucin secretion over 2 h. VIP (10−9 to 10−5 M) stimulated mucin secretion in a dose-dependent fashion. VIP-induced mucin secretion was partially blocked by a VIP receptor antagonist (a chimeric VIP-pituitary adenylate cyclase-activating peptide analog, VIP receptor antagonist) at a 10-fold excess concentration. At all concentrations tested, neither NG-nitro-l-arginine methyl ester, an inhibitor of NO synthase, nor S-nitroso- N-acetyl-penicillamine, an NO donor, had any significant effect on constitutive or VIP-induced mucus secretion. We conclude that VIP-stimulated mucin and lysozyme secretion was both time dependent and dose dependent and that NO neither stimulates nor inhibits mucus secretion in the ferret trachea.

Nitric oxide synthase inhibitors protect cerebellar Purkinje cells from zinc-induced cell loss in adult rat

2011 ◽  
Vol 41 (1) ◽  
pp. 25-31 ◽  
Author(s):  
Mehmet Fatih Gökçe ◽  
Süleyman Kaplan ◽  
Ayten Türkkani ◽  
Ramazan Kozan ◽  
Mustafa Ayyildiz ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Purkinje Cells ◽  
Cell Loss ◽  
Nitric Oxide Synthase Inhibitors ◽  
Adult Rat ◽  
Cerebellar Purkinje Cells ◽  
Oxide Synthase

The nitric oxide donor molsidomine prevents ischemia/reperfusion injury of the adult rat small intestine

2003 ◽  
Vol 19 (4) ◽  
pp. 305-308 ◽  
Author(s):  
Hayrettin Öztürk ◽  
Mustafa Aldemir ◽  
Ali İhsan Dokucu ◽  
Yusuf Yağmur ◽  
Nihal Kilinç ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nitric Oxide Donor ◽  
Rat Small Intestine ◽  
Adult Rat

Modulation of vasoactive intestinal peptide pulmonary relaxation by NO in tracheally superfused guinea pig lungs

1993 ◽  
Vol 265 (4) ◽  
pp. L410-L415 ◽  
Author(s):  
C. M. Lilly ◽  
J. S. Stamler ◽  
B. Gaston ◽  
C. Meckel ◽  
J. Loscalzo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Confidence Interval ◽  
Guinea Pig ◽  
Vasoactive Intestinal Peptide ◽  
Inhibitory Effect ◽  
Lung Perfusion ◽  
Perfusion Fluid ◽  
Oxide Synthase ◽  
Dependent Mechanism

The mechanism of vasoactive intestinal peptide (VIP)-induced pulmonary relaxation in tracheally perfused guinea pig lungs was defined with the use of inhibitors of nitric oxide synthase (NOS) and by direct measurement of nitric oxide (NO) equivalents recovered from lung perfusion fluid. Lungs treated with 200 microM NG-nitro-L-arginine were resistant to the relaxant effects of VIP in these lungs; the 50% inhibitory dose (ID50) for VIP was 32 nmol/kg (95% confidence interval, 16–79), which was approximately 100-fold greater than the ID50 of control lungs which was 0.39 nmol/kg, (0.16–0.79, P < 0.0001). This inhibitory effect could be overcome with excess L- but not D-arginine. In contrast, VIP-induced relaxation of isolated guinea pig trachea was not modified by inhibitors of NOS. To confirm that VIP infusion resulted in NO generation in whole lungs, we measured NO equivalents in lung effluent by two distinct technologies. We found that VIP injection caused a significant increase in NO equivalents from 0.11 +/- 0.04 microM to 0.78 +/- 0.15 microM (P < 0.05) and that this increase preceded VIP-induced pulmonary relaxation. Lungs pretreated with the putative guanylyl cyclase inhibitor methylene blue were less responsive to VIP [ID50 4.0 nmol/kg (1.5–10), P < 0.005 compared with control lungs], consistent with a physiologically significant guanosine 3',5'-cyclic monophosphate-dependent mechanism. Our data demonstrate that VIP has the capacity to relax whole lungs in part by stimulating the generation of NO.

Expression of nitric oxide synthase isoforms (NOS II and NOS III) in adult rat lung in hyperoxic pulmonary hypertension

1999 ◽  
Vol 295 (2) ◽  
pp. 317-329 ◽  
Author(s):  
Wolfgang Steudel ◽  
Masazumi Watanabe ◽  
Krikor Dikranian ◽  
Margaretha Jacobson ◽  
R. C. Jones
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Nitric Oxide Synthase ◽  
Rat Lung ◽  
Adult Rat ◽  
Oxide Synthase
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