Role of nitric oxide and vasoactive intestinal polypeptide in vagally mediated relaxation of the gastric corpus in the anaesthetized ferret

Grundy, David; Gharib-Naseri, Mohammad Kazem; Hutson, D. H.

doi:10.1016/0165-1838(93)90330-w

Cited by 58 publications

(37 citation statements)

References 13 publications

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“…Vagally induced relaxation was prevented by L-NAME, an inhibitor of NO formation and reversed by L-arginine, the substrate for NO formation, whereas the relaxation induced by VIP was unaffected by L-NAME or L-arginine. In Similarly, Lefebvre et al (1992) showed that in circular muscle strips of guinea pig gastric fundus N0-nitro-L-arginine shown that inhibition of NOS only partially prevents gastric relaxation in the rat and ferret (Li & Rand, 1990;Boeckxstaens et al, 1992;Grundy et al, 1993), findings that could be due variations in the relative importance of NO and VIP as inhibitory transmitters in different species and tissues. For instance, even though NO and VIP have been reported to be co-transmitters in the guinea pig trachea (Tucker et al, 1990;Li & Rand, 1991), NO is the main transmitter in feline and human trachea (Belvisi et al, 1992;Fisher et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

“…In addition, NOS has been localized to the vagal efferent fibres innervating the rat stomach (Forster & Southam, 1993). Histochemistry also suggests that NO is a neurotransmitter with paraneuronal actions in the brain (Schmidt et al, 1992), and recently NO release has been shown from isolated ganglia of the myenteric plexus of the guinea pig ileum (Grider & Jin, 1993 (VIP) has also been proposed as a mediator of gastric relaxation in the guinea pig, rat, cat and ferret (Grider et al, 1985;D'Amato et al, 1988D'Amato et al, , 1992Kamata et al, 1988;Grundy et al, 1993). For instance, electrical field stimulation of muscle strips from the guineapig and rat gastric fundus causes release of VIP-like immunoreactivity (Grider & Makhlouf, 1987;D'Amato et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

“…For instance, electrical field stimulation of muscle strips from the guineapig and rat gastric fundus causes release of VIP-like immunoreactivity (Grider & Makhlouf, 1987;D'Amato et al, 1992). It has also been suggested that VIP and NO are co-transmitters of gastric relaxation in the guinea pig, rat and ferret (Li & Rand, 1990;Boeckxstaens et al, 1992;Grider et al, 1992;Said, 1992;Grider & Jin, 1993;Grundy et al, 1993) and internal anal sphincter in the opossum (Chakder & Rattan, 1993). One possibility is that VIP acts partly through stimulation of NO formation, as has been suggested in the smooth muscle cells of the guinea pig stomach (Grider et al, 1992).…”

Section: Introductionmentioning

confidence: 99%

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Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Desai

Warner

Bishop

et al. 1994

British J Pharmacology

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Hammersmith Hospital, Du Cane Road, London W12 ONN 1 Nitric oxide synthase (NOS) The cross-sections of the stomach wall showed NOS-positive neurones mainly in the myenteric plexus ganglia and NOS-positive nerve fibre varicosities in the circular muscle layer. 4 Relaxations induced by vagal stimulation were almost completely prevented by L-NAME with an IC50 value of 5.5 x 10-6M. This inhibition was reversed by L-arginine (2 mM).5 VIP (100nM) induced reproducible relaxations of the stomach. These were unaffected by tetrodotoxin (2f1M) or Nw-nitro-L-arginine methyl ester (L-NAME, 100 AM).6 Desensitization to the relaxant effect of VIP partially reduced relaxations induced by vagal stimulation, glyceryl trinitrate or sodium nitroprusside but not noradrenaline. 7 These results show that NO has a neuronal origin in the guinea pig stomach, and support NO, and not VIP, as the major neurotranmitter of vagally induced gastric relaxation in the guinea pig.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Desai

Warner

Bishop

et al. 1994

British J Pharmacology

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“…It seems unlikely that the effect is limited to control of a particular organ system. The dual excitatory (i.e., cholinergic) and inhibitory (i.e., noncholinergic, nonadrenergic) pathways of the vagus peripherally allow for excitation and/or inhibition of DMV neurons to lead to inhibition of smooth muscle (D'Amato et al, 1992;Grundy et al, 1993;Desai et al, 1994;Paterson et al, 2000). Unfortunately, no evidence exists to directly correlate morphological or electrophysiological properties of individual DMV neurons with their final effect on the viscera, so it is currently impossible to determine in a slice preparation which functional vagal pathway is affected by a given DMV neuron.…”

Section: Discussionmentioning

confidence: 99%

Vanilloid-Mediated Heterosynaptic Facilitation of Inhibitory Synaptic Input to Neurons of the Rat Dorsal Motor Nucleus of the Vagus

Derbenev

Monroe²,

Glatzer³

et al. 2006

J. Neurosci.

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Vanilloid type-1 receptors (VR1) are abundant in the dorsal vagal complex, where their function is mostly unknown. We examined the role of VR1 in regulating synaptic inputs to neurons of the dorsal motor nucleus of the vagus (DMV). Using patch-clamp recordings from DMV neurons in brainstem slices, capsaicin was found to increase action potential-independent inhibitory input onto DMV neurons. This rapid effect was mimicked by application of the endogenous cannabinoid, anandamide and blocked by VR1 antagonists. The VR1-mediated facilitation of synaptic inhibition was reduced by ionotropic and metabotropic glutamate receptor antagonists, suggesting an indirect, heterosynaptic enhancement of GABA release caused by a VR1-mediated increase in glutamate release from presynaptic terminals of excitatory neurons. Application of L-glutamate also increased GABA release. The paired-pulse ratio was increased for IPSCs evoked after electrical stimulation of the nucleus tractus solitarius, but the effect was slower than for the enhancement of spontaneous and miniature IPSCs. Capsaicin also increased the frequency of glutamatergic postsynaptic currents in a VR1-mediated manner. Results of these studies suggest that VR1-containing glutamatergic terminals contact DMV neurons. Activation of VR1 potently enhances glutamate release onto GABAergic terminals, facilitating GABA release. Endogenous cannabinoids can thereby rapidly enhance inhibitory input to DMV neurons via VR1-mediated presynaptic mechanisms.

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“…Both vasoactive intestinal polypeptide (VIP) and nitric oxide (NO) have been proposed as NANC neurotransmitters in the proximal part of the stomach (Lefebvre, 1993). Whereas in species such as the rat and the ferret, NO is mainly involved in short-lasting relaxations and in initiating sustained relaxations (Li & Rand, 1990;D'Amato et al, 1992;Grundy et al, 1993), in other species such as the guinea-pig it is also the predominant neurotransmitter during sustained relaxation (Lefebvre et al, 1992a;Desai et al, 1994). The vagal preganglionic e erent ®bres to the stomach seem centrally organized in a reciprocal manner: when the e erents supplying the intramural cholinergic neurones are active, the discharge in those supplying the intramural inhibitory NANC neurones is suppressed, and vice versa (Andrews, 1990).…”

Section: Introductionmentioning

confidence: 99%

Investigation of the interaction between cholinergic and nitrergic neurotransmission in the pig gastric fundus

Leclere¹,

Lefebvre²

1998

British J Pharmacology

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1 The interaction between the cholinergic and nitrergic innervation was investigated in circular muscle strips of the pig gastric fundus. 2 In physiological salt solution containing 4610 76 M guanethidine, electrical ®eld stimulation (EFS; 40 V, 0.5 ms, 0.5 ± 32 Hz, 10 s at 4 min intervals) induced small transient relaxations at 0.5 ± 4 Hz, and large frequency-dependent contractions, sometimes followed by o -relaxations, at 8 ± 32 Hz. 3 In the presence of L-N G -nitroarginine methyl ester (L-NAME; 3610 74 M) or physostigmine (10 76 M), relaxations were reversed into contractions and contractions were enhanced. Physostigmine added to L-NAME further enhanced contractions, while addition of L-NAME to physostigmine had no additional e ect. O -relaxations were enhanced in the presence of L-NAME and physostigmine. L-NAME and physostigmine consistently increased basal tone. 4 Tissues contracted by 5-hydroxytryptamine or by acetylcholine responded to EFS in a similar way as in basal conditions and L-NAME reversed the relaxations at the lower stimulation frequencies into contractions and enhanced the contractions at the higher stimulation frequencies. 5 O -relaxations in the presence of L-NAME were partially reduced by a-chymotrypsin (10 U ml 71 ). 6 In the absence of physostigmine, the concentration-response curve to exogenous acetylcholine was not in¯uenced by L-NAME. 7 Contractions of the same amplitude induced by EFS at 4 Hz and by exogenous acetylcholine were either decreased or enhanced to the same extent by sodium nitroprusside (SNP; 10 75 M), depending upon the degree of relaxation by SNP. 8 These experiments suggest that endogenous nitric oxide interferes with cholinergic neurotransmission in the pig gastric fundus by functional antagonism at the postjunctional level. The interaction is independent of the degree of contraction.

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Role of nitric oxide and vasoactive intestinal polypeptide in vagally mediated relaxation of the gastric corpus in the anaesthetized ferret

Cited by 58 publications

References 13 publications

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Nitric oxide, and not vasoactive intestinal peptide, as the main neurotransmitter of vagally induced relaxation of the guinea pig stomach

Vanilloid-Mediated Heterosynaptic Facilitation of Inhibitory Synaptic Input to Neurons of the Rat Dorsal Motor Nucleus of the Vagus

Investigation of the interaction between cholinergic and nitrergic neurotransmission in the pig gastric fundus

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