Inhibition of tetrahydroisoxazolo-pyridin-3-ol and muscimol and its mechanism on gastrointestinal transit in mice

Subramanian, Ramaswamy; Srinivasan, Duraisamy; Js, Bapna

doi:10.1016/0014-2999(92)90742-m

Cited by 4 publications

(2 citation statements)

References 10 publications

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“…However, physiological significance of the UVA‐induced increase of DOPA‐ and HDC‐positive mast cells is not clear at present. It should be noted that exposure of animals to strong stressors significantly changed the balance of mucosal immune systems and intestinal peristalsis (26). This work shows that UVA irradiation to the eye significantly inhibited the peristalsis of the small intestine of control, hypophysectomized or iNOS −/− mice.…”

Section: Discussionmentioning

confidence: 99%

Ultraviolet‐A Irradiation to the Eye Modulates Intestinal Mucosal Functions and Properties of Mast Cells in the Mouse

Yamate

Hiramoto

Kasahara

et al. 2010

Photochem & Photobiology

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We previously reported that topical irradiation of the eye by ultraviolet-B (UVB) activated hypothalamo-pituitary-adrenal axis (HPA-A) of the mouse to increase 3, 4-dihydroxyphenylalanine (DOPA)-positive melanocytes in the skin by an inducible nitric oxide synthase (iNOS)-dependent mechanism. This work demonstrates that irradiation of the eye by ultraviolet-A (UVA) specifically increased DOPA-positive cells in the mucosa of the jejunum and colon of C57BL/6J mice by some HPA- and iNOS-independent mechanism. UVA-induced increase in DOPA-positive cells in the intestine was inhibited by the administration of hexamethonium or prazosin plus propranolol, blockers for the sympathetic nervous system. UVA irradiation of the eye increased DOPA- and histidine decarboxylase (HDC)-positive cells in the intestinal mucosa of both C57BL/6J and WBB6F1/J mice but not in the mutant strain W/Wv of the latter that lack mast cells. UVA irradiation of the eye suppressed the intestinal peristalsis of control, hypophysectomized or iNOS(-/-) C57BL/6J mice by the mechanism that was inhibited by hexamethonium or prazosin plus propranolol. These observations suggest that UVA irradiation of the eye stimulated the sympathetic nervous system to increase the mucosal DOPA- and HDC-positive mast cells and suppressed the peristalsis of the small intestine of the mouse.

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Section: Discussionmentioning

confidence: 99%

Ultraviolet‐A Irradiation to the Eye Modulates Intestinal Mucosal Functions and Properties of Mast Cells in the Mouse

Yamate

Hiramoto

Kasahara

et al. 2010

Photochem & Photobiology

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“…30 min before hemorrhage. This dose has previously been shown to produce ␣ -adrenergic blockade in mice, as determined by its effects on ␣ -adrenergic-induced alterations in intestinal transit (35), insulin secretion (36), and release of endogenous catecholamines (37).…”

Section: Interventionsmentioning

confidence: 99%

Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappaB regulation and cytokine expression.

et al. 1997

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The expression of proinflammatory and immunoregulatory cytokines rapidly increases in the lungs after hemorrhage, and such alterations contribute to the frequent development of acute inflammatory lung injury in this setting. Blood loss also produces elevations in catecholamine concentrations in the pulmonary and systemic circulation. In the present experiments, we used ␣ -and ␤ -adrenergic receptor blockade to examine in vivo interactions between hemorrhage-induced adrenergic stimulation and pulmonary cytokine expression. Treatment of mice with the ␣ -adrenergic receptor antagonist phentolamine prevented not only the elevation in mRNA levels of IL-1 ␤ , TNF-␣ , and TGF-␤ 1, the increase in IL-1 ␤ protein, but also the activation of nuclear factor (NF)-B and cyclic AMP response element binding protein, which occurred in lung cells of untreated animals during the first hour after hemorrhage. In contrast, treatment before hemorrhage with the ␤ -adrenergic receptor antagonist propranolol was associated with increases in mRNA levels for IL-1 ␤ , TNF-␣ , and TGF-␤ 1, which were greater than those present in untreated hemorrhaged mice, and did not prevent hemorrhage-associated increases in lung IL-1 ␤ protein. Treatment with propranolol prevented hemorrhageinduced phosphorylation of cyclic AMP response element binding protein, but increased hemorrhage-associated activation of NF-B. These results demonstrate that hemorrhage initially increases pulmonary cytokine expression through ␣ -but not ␤ -adrenergic stimulation, and suggest that such ␣ -adrenergic-mediated effects occur through activation of the transcriptional regulatory factor NF-B. ( J. Clin. Invest. 1997. 99:1516-1524.)

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α-Adrenergic blockade restores normal fluid transport capacity of alveolar epithelium after hemorrhagic shock

Laffon

Modelska

et al. 1999

American Journal of Physiology-Lung Cellular and Molecular Phys

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Activation of beta-adrenergic receptors in the lung is an important mechanism that can prevent alveolar flooding after brief but severe hemorrhagic shock. However, a neutrophil-dependent oxidant injury to the alveolar epithelium prevents the normal upregulation of alveolar fluid clearance by catecholamines after prolonged hemorrhagic shock. Because hemorrhage increases proinflammatory cytokine expression in the lung partly through the activation of alpha-adrenergic receptors, the objective of this study was to determine whether alpha-adrenergic blockade would restore the normal fluid transport capacity of the alveolar epithelium after hemorrhagic shock. Hemorrhagic shock was associated with a significant increase of interleukin-1beta (IL-1beta) concentration in the lung and a failure of the alveolar epithelium to respond to beta-adrenergic agonists, with the upregulation of vectorial fluid transport despite intra-alveolar administration of exogenous catecholamines. In contrast, catecholamine-mediated upregulation of alveolar liquid clearance was restored by pretreatment with phentolamine, an alpha-adrenergic-receptor antagonist. Phentolamine pretreatment also significantly attenuated the shock-mediated increase of IL-1beta concentration in the lung. Additional experiments demonstrated that the inhibition of IL-1beta binding to its receptor by the administration of IL-1-receptor antagonist restored the normal fluid transport capacity of the alveolar epithelium after hemorrhagic shock. In summary, the results of these studies indicate that the activation of alpha-adrenergic receptors after hemorrhagic shock prevents the beta-adrenergic-dependent upregulation of alveolar fluid clearance by modulating the severity of the pulmonary inflammatory response.

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Inhibition of tetrahydroisoxazolo-pyridin-3-ol and muscimol and its mechanism on gastrointestinal transit in mice

Cited by 4 publications

References 10 publications

Ultraviolet‐A Irradiation to the Eye Modulates Intestinal Mucosal Functions and Properties of Mast Cells in the Mouse

Ultraviolet‐A Irradiation to the Eye Modulates Intestinal Mucosal Functions and Properties of Mast Cells in the Mouse

Hemorrhage increases cytokine expression in lung mononuclear cells in mice: involvement of catecholamines in nuclear factor-kappaB regulation and cytokine expression.

α-Adrenergic blockade restores normal fluid transport capacity of alveolar epithelium after hemorrhagic shock

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