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.

Nitric oxide may be the final mediator of nonadrenergic, noncholinergic inhibitory junction potentials in the gut

1991 ◽  
Vol 69 (10) ◽  
pp. 1448-1458 ◽  
Author(s):  
Frank Christinck ◽  
Jennifer Jury ◽  
Francisco Cayabyab ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Methylene Blue ◽  
Vasoactive Intestinal Polypeptide ◽  
Time Course ◽  
Contractile Activity ◽  
Circular Muscle ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Sucrose Gap ◽  
Intestinal Polypeptide

This study tested the hypothesis that the final mediator of nonadrenergic, noncholinergic (NANC) inhibitory junction potentials (ijps) and associated relaxation responses was nitric oxide (NO) or a related substance and not vasoactive intestinal polypeptide (VIP). We used opossum esophagus body circular muscle and canine intestine circular muscle. In both these tissues, ijps had reversal potentials near the potassium equilibrium potential, (EK); in esophagus the ijps were apamin insensitive, but in the intestine they were partially apamin sensitive. Nω-Nitro-L-arginine methyl ester (NAME) (10−5 to 5 × 10−4 M) abolished ijps in both tissues, an effect overcome by 10−3 M L-arginine but not D-arginine. NAME increased input resistance of esophagus tissues in the double sucrose gap but caused no significant depolarization in the sucrose gap or in studies with microelectrodes. Contractions and basal tension were increased in both tissues by NAME. The apamin sensitive and insensitive ijp components in canine muscle were both abolished by NAME, but the time course of this abolition was different for the two components. Methylene blue (10–50 μM) with variable rapidity and extent inhibited ijps in both tissues, but L-arginine could not overcome this effect. Methylene blue, like NAME, did not depolarize detectably but enhanced the contractile activity. VIP (10−6 M) had very small effects in both tissues, little or no hyperpolarization and increased input resistance in esophagus, these effects were not changed by NAME, and VIP did not affect ijps. We conclude that NO may be the final mediator of NANC-initiated inhibitory junction potentials in gastrointestinal circular smooth muscle.Key words: nitric oxide, nonadrenergic noncholinergic inhibitory mediator, vasoactive intestinal polypeptide, esophagus, intestine.

scholarly journals Role of nitric oxide- and vasoactive intestinal polypeptide-containing neurones in human gastric fundus strip relaxations

2000 ◽  
Vol 129 (1) ◽  
pp. 12-20 ◽  
Author(s):  
M Tonini ◽  
R De Giorgio ◽  
F De Ponti ◽  
C Sternini ◽  
V Spelta ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Vasoactive Intestinal Polypeptide ◽  
Gastric Fundus ◽  
Intestinal Polypeptide

Efffect of vasoactive intestinal polypeptide on gallbladder smooth muscle in vitro.

1978 ◽  
Vol 234 (1) ◽  
pp. E44 ◽  
Author(s):  
J P Ryan ◽  
S Ryave
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Motor Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Muscle Tone ◽  
Contractile Activity ◽  
Gastrointestinal Hormones ◽  
Resting Tension ◽  
Intestinal Polypeptide

The effect of vasoactive intestinal polypeptide (VIP) on basal and octapeptide of cholecystokinin (OP-CCK) induced tension was examined with guinea pig gallbladder smooth muscle strips in vitro. VIP alone produced dose-related decreases in resting tension and antagonized spontaneous contractile activity where present. In combination with OP-CCK, VIP decreased the expected contractile respone. The degree of antagonism depended upon the concentrations of OP-CCK and VIP. VIP had no effect on acetylcholine-induced contractions. From these observations, we propose that VIP can affect gallbladder motor activity by decreaseing smooth muscle tone and by antagonizing cholecystokinin. These findings lend further support to our proposal that gallbladder motor function may depend upon the action and interaction of the gastrointestinal hormones.

scholarly journals Development-Dependent Plasticity in Vasoactive Intestinal Polypeptide Neurons in the Infralimbic Cortex

2021 ◽  
Vol 2 (1) ◽  
Author(s):  
Stuart A Collins ◽  
Ipe Ninan
Keyword(s):  
Sex Differences ◽  
Anxiety Disorders ◽  
Vasoactive Intestinal Polypeptide ◽  
Cortical Plasticity ◽  
Male Mice ◽  
Infralimbic Cortex ◽  
Membrane Excitability ◽  
Gabaergic Transmission ◽  
Intestinal Polypeptide

Abstract The onset of several neuropsychiatric disorders including anxiety disorders coincides with adolescence. Consistently, threat extinction, which plays a key role in the regulation of anxiety-related behaviors, is diminished during adolescence. Furthermore, this attenuated threat extinction during adolescence is associated with an altered synaptic plasticity in the infralimbic medial prefrontal cortex (IL-mPFC), a brain region critical for threat extinction. However, the mechanism underlying the altered plasticity in the IL-mPFC during adolescence is unclear. Given the purported role of vasoactive intestinal polypeptide expressing interneurons (VIPINs) in disinhibition and hence their potential to affect cortical plasticity, we examined whether VIPINs exhibit an adolescence-specific plasticity in the IL-mPFC. We observed an increase in GABAergic transmission and a decrease in excitability in VIPINs during adolescence. Male mice show a significantly higher VIPIN-pyramidal neuron GABAergic transmission compared with female mice. The observed increase in GABAergic transmission and a decrease in membrane excitability in VIPINs during adolescence could play a role in the altered plasticity in the adolescent IL-mPFC. Furthermore, the suppression of VIPIN-mediated GABAergic transmission in females might be relevant to sex differences in anxiety disorders.

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