Involvement of nitric oxide in non-adrenergic non-cholinergic relaxation and action of vasoactive intestinal polypeptide in circular muscle strips of the rat gastric fundus

2001 ◽  
Vol 44 (3) ◽  
pp. 221-228 ◽  
Author(s):  
Yusuf Ergün ◽  
Nuran Ö gülener ◽  
Atilla Dikmen
Keyword(s):  
Nitric Oxide ◽  
Vasoactive Intestinal Polypeptide ◽  
Circular Muscle ◽  
Gastric Fundus ◽  
Rat Gastric Fundus ◽  
Intestinal Polypeptide

scholarly journals Release of vasoactive intestinal polypeptide from the rat gastric fundus

1992 ◽  
Vol 105 (3) ◽  
pp. 691-695 ◽  
Author(s):  
M. D'Amato ◽  
D. Currò ◽  
P. Montuschi ◽  
G. Ciabattoni ◽  
E. Ragazzoni ◽  
...  
Keyword(s):  
Vasoactive Intestinal Polypeptide ◽  
Gastric Fundus ◽  
Rat Gastric Fundus ◽  
Intestinal Polypeptide

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.

Sign in / Sign up

Export Citation Format

Share Document