Expression and activation of β-adrenoceptors in the colorectal mucosa of rat and human

Zhang, X. H.; Ji, Tuo; Guo, Hongwei; Liu, Sumei; Li, Y.; Zheng, Li‐Fei; Zhang, Y.; Zhang, X. F.; Duan, Zhongping; Zhu, Jinxia

doi:10.1111/j.1365-2982.2010.01598.x

Cited by 20 publications

(9 citation statements)

References 37 publications

(57 reference statements)

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“…Of note, propranolol also produced a significant reduction in energy expenditure in the S-5AA, S-5AA+Met, and S-16AA-Met. Because 6-OHDA treatment increases the protein abundance of β1 and β2-AR in the colon with enhanced sensitivity to dopamine and norepinephrine to colonic ion transport [59], it is likely that the upregulation of peripheral β1 and β2-AR contributed to the robust effects of propranolol on energy expenditure in 6-OHDA-treated rats. Alternatively, it is also likely that 6-OHDA was ineffective in producing a total ablation of noradrenergic nerve terminals with the subsequent recovery of β-adrenergic signaling over the 3-week course of the study.…”

Section: Discussionmentioning

confidence: 99%

Methionine Restriction Partly Recapitulates the Sympathetically Mediated Enhanced Energy Expenditure Induced by Total Amino Acid Restriction in Rats

et al. 2019

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Total amino acid (AA) restriction promotes hyperphagia and energy expenditure. We determined whether (i) methionine restriction mimics the effects of total AA restriction, (ii) methionine supplementation attenuates these responses, and iii) sympathetic signaling mediates such effects. Rats were injected with either vehicle (V) or 6-hydroxydopamine (S) to induce chemical sympathectomy, and then randomized to four diets: 16% AA (16AA), 5% AA (5AA), 16% AA-methionine (16AA-Met), and 5% AA+methionine (5AA+Met). Propranolol or ondansetron were injected to examine the role of sympathetic and serotonergic signaling, respectively. 5AA, 5AA+Met, and 16AA-Met increased the food conversion rate for 1–3 weeks in the V and S groups, and increased mean energy expenditure in V group,; the magnitude of these changes was attenuated in the S group. Propranolol decreased the energy expenditure of V16AA, V5AA, and V5AA+Met and of S5AA, S5AA+Met, and S16AA-Met, whereas ondansetron decreased the energy expenditure in only the S groups. Compared to 16AA, the other V groups had reduced body weights from days 7–11 onwards and decreased lean masses throughout the study and the other S groups had decreased body weights and lean masses from day 14 onwards. Total AA restriction enhanced the energy expenditure and reduced the weight and lean mass; these effects were partly recapitulated by methionine restriction and were sympathetically mediated.

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Section: Discussionmentioning

confidence: 99%

Methionine Restriction Partly Recapitulates the Sympathetically Mediated Enhanced Energy Expenditure Induced by Total Amino Acid Restriction in Rats

et al. 2019

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“…Indeed, dopaminergic blockers (domperidone, for example) are used as GI prokinetics, as they antagonize DA inhibitory effects on GI motility, by blocking DRD2 . A further element of complexity is added by the observation that, in the GI, DA is able to activate adrenergic (alpha and beta) receptors to modulate, for example, motility in the small intestine and ion transport in the distal colon …”

Section: Discussionmentioning

confidence: 99%

“…With DRD2 being blocked by L‐741626, overabundant endogenous DA may have activated alternative, non‐dopaminergic receptors, causing peristalsis inhibition. Indeed, various studies have shown that DA can activate beta‐adrenergic receptors in various GI segments, including the distal colon and activation of beta‐adrenergic receptors is associated with muscle relaxation . Moreover, it has been reported that L‐741626, while blocking DRD2, can enhance DA release, for example in the striatum of rats or in the guinea‐pig cochlea .…”

Section: Discussionmentioning

confidence: 99%

Response of colonic motility to dopaminergic stimulation is subverted in rats with nigrostriatal lesion: relevance to gastrointestinal dysfunctions in Parkinson's disease

Levandis

Balestra

Siani

et al. 2015

Neurogastroenterology Motil

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“…Furthermore, the presence of mRNA for β1/2/3‐AR in rat vaginal epithelium and β1/2‐AR in VK2E6E7 cells were indentified. As epithelial β3‐AR is neither expressed in VK2/E6E7 cells nor involved in ion transport [40], the β1/2‐AR protein expression was examined by Western blot and immunofluorescence. The observations above suggested that the epithelial β1‐AR and β2‐AR are both expressed in vaginal epithelium and involved in mediating adrenaline‐induced Cl − secretion.…”

Section: Discussionmentioning

confidence: 99%

Activation of β-Adrenergic Receptors During Sexual Arousal Facilitates Vaginal Lubrication by Regulating Vaginal Epithelial Cl− Secretion

Sun

Huang

Yang

et al. 2014

The Journal of Sexual Medicine

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Introduction Vaginal lubrication, an indicator of sexual arousal and tissue health, increases significantly during genital sexual arousal. Adrenergic alpha-receptors (AR) are an important regulator of genital physiological responses involved in mediating vascular and nonvascular smooth muscle contractility; the role of β-AR in sexual arousal, however, has not yet been investigated. Aim The goal of this study was to reveal the functional role of β-AR in modulating vaginal lubrication during sexual arousal and the mechanisms underlying the process. Methods The effects of adrenaline on vaginal epithelial ion transport, intracellular cyclic adenosine monophosphate (cAMP) content ([cAMP]i), and vaginal lubrication were investigated using short-circuit current (ISC) of rat vaginas incubated in vitro, enzyme-linked immunosorbent assay (ELISA), and measurement of vaginal lubrication in vivo, respectively. The expressions of β-AR in vaginal epithelium were analyzed by reverse transcription-polymerase chain reaction, western blot, and immunofluorescence. Main Outcome Measures Changes of ISC responses; mRNA, protein expressions and localization of β-AR; [cAMP]i; vaginal lubrication. Results Serosal application of adrenaline induced an increase of ISC across rat vaginal epithelium that blocked by propranolol, a β-AR antagonist, rather than phentolamine, an α-AR antagonist. β1/2-AR were both present in rat and human vaginal epithelial cells. Removing Cl− or application of CFTR(inh)-172, an inhibitor of cystic fibrosis transmembrane conductance regulator (CFTR), abolished adrenaline-induced ISC responses. The elevated levels of [cAMP]i induced by adrenaline were prevented by the pretreatment with propranolol. Vaginal lubrication measured in vivo showed that adrenaline or pelvic nerve stimulation caused a marked increase in vaginal lubrication, whereas pretreatment with propranolol or CFTR(inh)-172 reduced the effect. Conclusions Activation of epithelial β-AR facilitates vaginal lubrication during sexual arousal by stimulating vaginal epithelial Cl− secretion in a cAMP-dependent pathway. Thus, vaginal epithelial β-AR might be another regulator of vaginal sexual arousal responses.

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Expression and activation of β-adrenoceptors in the colorectal mucosa of rat and human

Abstract: β₁- and β₂-adrenoceptors are predominantly expressed in the colorectal mucosa. Perturbation of endogenous catecholamine levels influences the expression and activation of β-adrenoceptors in the colorectal region.

Cited by 20 publications

References 37 publications

Methionine Restriction Partly Recapitulates the Sympathetically Mediated Enhanced Energy Expenditure Induced by Total Amino Acid Restriction in Rats

Methionine Restriction Partly Recapitulates the Sympathetically Mediated Enhanced Energy Expenditure Induced by Total Amino Acid Restriction in Rats

Response of colonic motility to dopaminergic stimulation is subverted in rats with nigrostriatal lesion: relevance to gastrointestinal dysfunctions in Parkinson's disease

Activation of β-Adrenergic Receptors During Sexual Arousal Facilitates Vaginal Lubrication by Regulating Vaginal Epithelial Cl− Secretion

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