Nitric oxide modulates release of noradrenaline in guinea-pig gastric fundus

Sotirov, E.; Papasova, M

doi:10.1016/s0361-9230(99)00264-6

Cited by 6 publications

(4 citation statements)

References 62 publications

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“…Therefore, NO seems to have a facilitatory role in the release of sympathetic neurotransmitters. In the isolated guinea pig gastric fundus previously incubated with 3 H-norepinephrine, the nicotinic agonist DMPP or electrical field stimulation caused an increase in the 3 H overflow, and this effect was suppressed by L-NA, suggesting that endogenous NO increases the release of norepinephrine from adrenergic nerves (Sotirov and Papasova, 2000). In contrast, NO inhibits (Greenberg et al, 1990) or does not affect (Toda et al, 1990b;Bucher et al, 1992;Pa et al, 1992) the release of norepinephine from adrenergic nerves in blood vessels.…”

Section: Prejunctional Regulationmentioning

confidence: 99%

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Toda

Herman

2005

Pharmacol Rev

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Section: Prejunctional Regulationmentioning

confidence: 99%

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Toda

Herman

2005

Pharmacol Rev

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“…The neurally dependent response of the guinea‐pig stomach fundus comprises of an acetylcholine‐dependent contractile component (blockable by atropine), and a relaxatory one which is believed to depend on the release of NO (at stimulation frequencies below 10 Hz) and vasoactive intestinal polypeptide (at stimulation frequencies above 10 Hz). Thus, at stimulation frequencies between 1 and 5 Hz, NO is practically the only relaxatory neurotransmitter to be released by EFS in this tissue (Sotirov et al . 1999, Sotirov & Papasova 2000).…”

Section: Contraction Studiesmentioning

confidence: 99%

Induction of heme oxygenase in guinea‐pig stomach: roles in contraction and in single muscle cell ionic currents

Kadinov¹,

Itzev²,

Gagov³

et al. 2002

Acta Physiologica Scandinavica

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The role of heme oxygenase reaction products in modulation of stomach fundus excitability was studied. The presence of constitutive heme oxygenase 2 was verified in myenteric ganglia by immunohistochemistry. The role of inducible heme oxygenase isoenzyme was investigated after invivo treatment of animals with CoCl2 (80 mg kg-1 b.w) injected subcutaneously 24 h before they were killed. This treatment resulted in increased production of bilirubin and positive staining for the inducible isoform in stomach smooth muscle and vast induction in the liver. In both control and treated animals haemin, applied to the bath as a substrate of heme oxygenase caused significant decrease of prostaglandin F2alpha-induced tone, and ameliorated the relaxatory response of the fundic strips to electrical field stimulation. Both effects were antagonized by Sn-protoporphyrin IX, competitive heme oxygenase inhibitor, and were found to be neuronally dependent. In single freshly isolated smooth muscle cells from control animals haemin caused a concentration-dependent increase of the whole cell K+ currents, which was not affected by Sn-protoporphyrin IX, cyclic guanosine monophosphate (cGMP)-dependent protein kinase or guanylyl cyclase antagonists, but was reversed by various antioxidants and abolished by an NO scavenger. In cells from treated animals the K+ current increasing effect of haemin did not depend on the presence of antioxidants, but was abolished by protein kinase G and guanylyl cyclase inhibitors, depletors of intracellular Ca2+ pools or Sn-protoporphyrin IX. Biliverdin did not affect contraction or ionic currents. Thus, this is the first study demonstrating that heme oxygenase is an inducible enzyme in guinea-pigs, which exerts a modulatory role on gastric smooth muscle excitability via carbon monoxide production.

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“…Investigators found that cholinergic neurons stimulate the NA neurons to release NA in the VMH [116]. Since glucose levels, through GI neurons, inversely regulate NO levels [117], and since NO causes ACh release [118], this suggests that during hypoglycaemia, through NO, GI neurons activate a neuronal cascade involving cholinergic, noradrenernaline and GABAergic neurons in the VMH which mediate the process that ultimately blunts the AR. …”

Section: A Heuristic Theory On the Mechanisms Of The Bsarmentioning

confidence: 99%

Mechanisms of the Blunting of the Sympatho-Adrenal Response: A Theory

Parekh

2009

CDR

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Development of therapeutic measures to reduce the risk of potentially fatal episodes of hypoglycaemia and thus to achieve the full benefits of intensive insulin therapy in diabetic patients requires a complete understanding of the multifactorial mechanisms for repeated hypoglycaemia-induced blunting of the sympatho-adrenal response (BSAR). After critical analysis of the hypotheses, this review paper suggests a heuristic theory. This theory suggests two mechanisms for the BSAR, each involving a critical role for the central brain noradrenergic system. Furthermore, this theory also suggests that the lateral hypothalamus (LH) plays an important role in this phenomenon. Within the framework of this theory, explanations for 1) sexual dimorphism in the adrenomedullary response (AR), 2) dissociation in the blunting of the AR and the sympathetic response (SR) and 3) antecedent exercise-induced blunting of the AR are provided. In addition, habituation of orexin-A neurons is suggested to cause defective awakening. Moreover, potential therapeutics measures have been also suggested that will reduce or prevent severe episodes of hypoglycaemia.

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Nitric oxide modulates release of noradrenaline in guinea-pig gastric fundus

Cited by 6 publications

References 62 publications

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Gastrointestinal Function Regulation by Nitrergic Efferent Nerves

Induction of heme oxygenase in guinea‐pig stomach: roles in contraction and in single muscle cell ionic currents

Mechanisms of the Blunting of the Sympatho-Adrenal Response: A Theory

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