Role of nitric oxide in the contraction of circular muscle in the rat portal vein

2000 ◽  
Vol 440 (3) ◽  
pp. 435-439 ◽  
Author(s):  
Keiichi Shimamura ◽  
Li-Bo Zou ◽  
Kyoko Matsuda ◽  
Fumiko Sekiguchi ◽  
Kazuo Yamamoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Portal Vein ◽  
Circular Muscle ◽  
Rat Portal Vein

scholarly journals INHIBITORY ROLE OF NITRIC OXIDE IN THE CONTRACTION OF RAT PORTAL VEIN

1997 ◽  
Vol 75 ◽  
pp. 50
Author(s):  
F. Sekiguchi ◽  
L.-B. Zou ◽  
K. Matsuda ◽  
K. Shimamura ◽  
K. Yamamoto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Portal Vein ◽  
Rat Portal Vein ◽  
Inhibitory Role

scholarly journals Loss of nitric oxide-mediated inhibition of purine neurotransmitter release in the colon in the absence of interstitial cells of Cajal

2017 ◽  
Vol 313 (5) ◽  
pp. G419-G433 ◽  
Author(s):  
Leonie Durnin ◽  
Andrea Lees ◽  
Sheerien Manzoor ◽  
Kent C. Sasse ◽  
Kenton M. Sanders ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interstitial Cells Of Cajal ◽  
Colonic Motility ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Interstitial Cells ◽  
Partial Loss ◽  
Purinergic Neurotransmission ◽  
Cells Of Cajal

Regulation of colonic motility depends on the integrity of enteric inhibitory neurotransmission mediated by nitric oxide (NO), purine neurotransmitters, and neuropeptides. Intramuscular interstitial cells of Cajal (ICC-IM) and platelet-derived growth factor receptor-α-positive (PDGFRα+) cells are involved in generating responses to NO and purine neurotransmitters, respectively. Previous studies have suggested a decreased nitrergic and increased purinergic neurotransmission in KitW/KitW-v ( W/Wv) mice that display lesions in ICC-IM along the gastrointestinal tract. However, contributions of NO to these phenotypes have not been evaluated. We used small-chamber superfusion assays and HPLC to measure the spontaneous and electrical field stimulation (EFS)-evoked release of nicotinamide adenine dinucleotide (NAD+)/ADP-ribose, uridine adenosine tetraphosphate (Up4A), adenosine 5′-triphosphate (ATP), and metabolites from the tunica muscularis of human, monkey, and murine colons and circular muscle of monkey colon, and we tested drugs that modulate NO levels or blocked NO receptors. NO inhibited EFS-evoked release of purines in the colon via presynaptic neuromodulation. Colons from W/Wv, Nos1−/−, and Prkg1−/− mice displayed augmented neural release of purines that was likely due to altered nitrergic neuromodulation. Colons from W/Wv mice demonstrated decreased nitrergic and increased purinergic relaxations in response to nerve stimulation. W/Wv mouse colons demonstrated reduced Nos1 expression and reduced NO release. Our results suggest that enhanced purinergic neurotransmission may compensate for the loss of nitrergic neurotransmission in muscles with partial loss of ICC. The interactions between nitrergic and purinergic neurotransmission in the colon provide novel insight into the role of neurotransmitters and effector cells in the neural regulation of gastrointestinal motility. NEW & NOTEWORTHY This is the first study investigating the role of nitric oxide (NO) and intramuscular interstitial cells of Cajal (ICC-IM) in modulating neural release of purines in colon. We found that NO inhibited release of purines in human, monkey, and murine colons and that colons from KitW/KitW-v ( W/Wv) mice, which present with partial loss of ICC-IM, demonstrated augmented neural release of purines. Interactions between nitrergic and purinergic neurotransmission may affect motility in disease conditions with ICC-IM deficiencies.

Role of nitric oxide-related inhibition in intestinal function: relation to vasoactive intestinal polypeptide

1994 ◽  
Vol 266 (1) ◽  
pp. G31-G39 ◽  
Author(s):  
E. E. Daniel ◽  
C. Haugh ◽  
Z. Woskowska ◽  
S. Cipris ◽  
J. Jury ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Motor Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Contractile Activity ◽  
Low Frequency ◽  
Circular Muscle ◽  
Arginine Infusion ◽  
Intestinal Segments ◽  
Intestinal Polypeptide

This study examined the role of nitric oxide (NO) in tonic inhibition of motor activity in isolated, perfused canine ileal segments. Brief addition of N omega-nitro-L-arginine methyl ester (L-NAME) to the perfusate caused, after a delay, a concentration-dependent persistent increase in tonic and phasic activity of circular muscle. This increased motor activity was prevented or reversed by addition of L- but not D-arginine to the perfusate. Removal of Ca2+ or addition of 10(-7) M omega-conotoxin (GVIA) to the perfusate markedly reduced this response. The motor activity induced by L-NAME was accompanied by loss of distal inhibition and enhanced excitation to low-frequency field stimulation. L-NAME infusion significantly reduced tonic vasoactive intestinal polypeptide (VIP) output, sodium nitroprusside increased VIP output, but L-arginine infusion did not restore VIP output. Atropine (10(-7) M) and/or hexamethonium (10(-4) M) reduced the motor response to L-NAME by 75%. Atropine reduced and hexamethonium nearly abolished VIP output. We conclude that there is tonic Ca(2+)-dependent NO output from perfused intestinal segments dependent on nerves with N-Ca channels, that NO acts to inhibit muscle directly and by inhibiting release of excitatory mediators, and that this output is the primary inhibitory determinant of contractile activity.

Enteric inhibitory neural regulation of human colonic circular muscle: Role of nitric oxide

1993 ◽  
Vol 105 (4) ◽  
pp. 1009-1016 ◽  
Author(s):  
Kathleen D. Keef ◽  
Chuang Du ◽  
Sean M. Ward ◽  
Byron McGregor ◽  
Kenton M. Sanders
Keyword(s):  
Nitric Oxide ◽  
Circular Muscle ◽  
Neural Regulation
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