Involvement of nitric oxide synthetic pathway in inhibitory junction potentials in canine proximal colon

Dalziel, H. H.; Thornbury, K. D.; Ward, Sean M.; Sanders, Kenton M.

doi:10.1152/ajpgi.1991.260.5.g789

Cited by 63 publications

(49 citation statements)

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“…Neurona l NOS is distributed throughout the myenteric plexus in the rat gut from stomach to distal colon (25), acting Heart/pup wt, ( X lO as an import ant mediator of relaxation of the esophagus (26), stomach (27), intestine (28), colon (29), and pylorus (30). The excitatory inner vation of the pylorus is largely cholinergic from the vaga l nerve (31).…”

Section: Discussionmentioning

confidence: 99%

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

et al. 1995

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Administration of the nitric oxide synthase (NOS) inhibitor, AP-nitro-L-arginine methyl ester (L-NAME) during pregnancy has been shown to compromise fetal growth. This study was designed to determine whether aminoguanidine, a predominate inhibitor of inducible NOS, affects fetal outcome. In addition, we extended the prenatal administration of L-NAME into the postnatal period (14 d) to determine whether neonatal growth and maturation were also affected. L-NAME, but not aminoguanidine, compromises fetal and placental growth. When compared with control 14-d-old pups, postnatal L-NAMEcompromised neonatal growth, whether it was given directly (intraperitoneally) (39.7 ± 1.1 versus 24.1 ± 1.0 g) or indirectly (38.6 ± 0.5 versus 22.2 ± 1.2 g) via maternal breast milk. Neonatal growth retardation was asymmetric, with brain sparing, suggesting a nutritional origin. L-NAME administration resulted in growth retardation that extended into adulthood, without evidence of catch-up growth. Treated neonates displayed the hallmarks of hypertrophic pyloric stenosis. Significant increases in stomach weight/pup weight (9.9 ± 0.3 versus 8.2 ± 0.4 X 10 3 ) and stomach volume/pup weight (12.0 ± 0.6 versus 9.4 ± 0.6 mL/100 g) with a concomitant Endogenous NO produced from L-arginine by NOS (1), is an important regulator in a number of physiologic proce sse s. Se veral different isoforms of NOS exist; the con stitutive isoforms regul ate v ascular tone (1), neurotransmission (2), and platelet aggregation (3), w hereas the ind ucible for m appears to have its primary effect s on inflammation (4, 5) and host defense (6). A number of exog enous NOS inhibitors have been identified including the structural an alog of L-arginine, I.-NA ME, w hich inhibits both co nstitutive and inducible NOS isoforms , wi th pr eference for the constitut ive isoform (7,8 Supported in parI by National Institutes of Health Granl ROI HD31885 (to MJ.S.M.) and American Heart Association, Louisiana Chapter (to M.R.P.). decrease in small intestine weight/length (2.10 ± 0.08 versus 3.18 ± 0.13 g/100 em) was noted in treated versus control pups (p < 0.05). Muscularis hypertrophy at the pyloric sphincter in the L-NAME-treated pups was noted by histology. Blood pressure was elevated in the L-NAME-treated pups (93 ± 6 versus 60 ± 5 mm Hg in control pups, p < 0.05). These findings are consistent with inhibition of neuronal and endothelial NOS activity. We conclude that NO, formed via the constitutive isoforms of NOS, is a critical determinant of fetal and neonatal growth and maturation. (Pediatr Res 38: 768-774, 1995) Abbreviations NO, nitric oxide NOS, nitric oxide synthase cNOS, constitutive nitric oxide synthase iNOS, inducible nitric oxide synthase L-NAME, AP-nitro-L-arginine methyl ester HPS , hypertrophic pyloric stenosis VIP , vasoactive intestinal polypeptide nidine, although not a i-arginine anal og, predominately inhibits the indu cible NOS isoform (9) .NO fo rma tion is up-regul ated in pregn ancy (10). Th e uteroplacental unit via both co nst itutive and ind...

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Section: Discussionmentioning

confidence: 99%

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

et al. 1995

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“…Pharmacological experiments revealed the first component to be dependent on activation of small-conductance, Ca 2ϩ -activated K ϩ channels and to be induced by purines (2,10,21,35). The second component is blocked by inhibitors of nitric oxide synthase (NOS) and is therefore regarded as nitrergic (5,23,31). This characteristic biphasic IJP has been shown for several other regions of the GI tract of different species as well, such as antrum (15), small intestine (12), and internal anal sphincter (6,30).…”

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confidence: 93%

Interstitial cells of Cajal mediate nitrergic inhibitory neurotransmission in the murine gastrointestinal tract

Lies

Gil

Groneberg

et al. 2014

American Journal of Physiology-Gastrointestinal and Liver Physi

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(ICC), and fibroblast-like cells. Up to date, the interplay between neurons and these cells to initiate a nitrergic inhibitory junction potential (IJP) is unclear. Here, we investigate the origin of the nitrergic IJP in murine fundus and colon. IJPs were determined in fundus and colon SMC of mice lacking NO-GC globally (GCKO) and specifically in SMC (SM-GCKO), ICC (ICC-GCKO), and both SMC/ICC (SM/ICC-GCKO). Nitrergic IJP was abolished in ICC-GCKO fundus and reduced in SM-GCKO fundus. In the colon, the amplitude of nitrergic IJP was reduced in ICC-GCKO, whereas nitrergic IJP in SM-GCKO was reduced in duration. These results were corroborated by loss of the nitrergic IJP in global GCKO. In conclusion, our results prove the obligatory role of NO-GC in ICC for the initiation of an IJP. NO-GC in SMC appears to enhance the nitrergic IJP, resulting in a stronger and prolonged hyperpolarization in fundus and colon SMC, respectively. Thus NO-GC in both cell types is mandatory to induce a full nitrergic IJP. Our data from the colon clearly reveal the nitrergic IJP to be biphasic, resulting from individual inputs of ICC and SMC.

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“…by drugs which inhibit the synthesis of NO, such as NG-nitro-L-arginine (L-NOARG) or NG-nitro-L-arginine methylester (L-NAME) (Moncada et al, 1991), suggests an important role of NO in the generation of the ij.p. (Dalziel et al, 1991;Sanders & Ward, 1992;Makhlouf & Grider, 1993). Contribution of NO to the generation of the ij.p.…”

Section: Introductionmentioning

confidence: 99%

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

Ohno

Lü

Yamamoto

et al. 1996

British J Pharmacology

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1 In circular smooth muscle of the guinea-pig gastric fundus, transmural nerve stimulation evoked a cholinergic excitatory junction potential (ej.p.), and blockade of the ej.p. by atropine revealed a nonadrenergic non-cholinergic (NANC) inhibitory junction potential (ij.p.).2 The amplitude of the ej.p. was increased by apamin, suramin or NGnitro-L-arginine (L-NOARG), with no significant change in the membrane potential. 3 The ij.p. consisted of two components (fast and slow); apamin inhibited the former, nitroarginine inhibited the latter, and suramin inhibited both components. 4 Apamin inhibited the hyperpolarization produced by adenosine 5'-triphosphate (ATP) but not by vasoactive intestinal polypeptide (VIP). Suramin inhibited the hyperpolarization produced by VIP but not by ATP. The sodium nitroprusside (SNP)-induced hyperpolarization was not blocked by apamin or suramin. L-NOARG or tetrodotoxin did not inhibit the hyperpolarization produced by ATP, VIP or SNP. 5 The data did not support the hypothesis that ATP, VIP or nitric oxide (NO) is the main transmitter responsible for generation of the NANC ij.p. in the fundus. 6 Actions of L-NOARG suggest that endogenous NO may be involved in junctional transmission, mainly as an inhibitory modulator of cholinergic transmission.

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Involvement of nitric oxide synthetic pathway in inhibitory junction potentials in canine proximal colon

Cited by 63 publications

References 0 publications

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

Perinatal Nitric Oxide Synthase Inhibition Retards Neonatal Growth by Inducing Hypertrophic Pyloric Stenosis in Rats

Interstitial cells of Cajal mediate nitrergic inhibitory neurotransmission in the murine gastrointestinal tract

Properties of the inhibitory junction potential in smooth muscle of the guinea‐pig gastric fundus

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