Parasympathetic Innervation

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A V Edwards - One of the best experts on this subject based on the ideXlab platform.

  • submandibular responses to stimulation of the Parasympathetic Innervation in anesthetized sheep
    Journal of Applied Physiology, 2003
    Co-Authors: C M B Edwards, P P Corkery, A V Edwards
    Abstract:

    Submandibular secretory and vascular responses to stimulation of the Parasympathetic Innervation and the output of vasoactive intestinal peptide (VIP) were investigated in anaesthetized sheep in th...

  • Submandibular responses to stimulation of the Parasympathetic Innervation in anesthetized sheep.
    Journal of Applied Physiology, 2003
    Co-Authors: C M B Edwards, P P Corkery, A V Edwards
    Abstract:

    Submandibular secretory and vascular responses to stimulation of the Parasympathetic Innervation and the output of vasoactive intestinal peptide (VIP) were investigated in anaesthetized sheep in the presence and absence of atropine (≥0.5 mg/kg). In the absence of atropine, Parasympathetic stimulation caused an increase in the flow of saliva and a decrease in submandibular vascular resistance; the latter response persisted after the administration of atropine and was then significantly reduced at the lowest but not at the higher frequencies tested. The output of VIP from the gland was frequency dependent over the range of 10-20 Hz (continuously) and significantly increased after atropine (P < 0.02). Furthermore, the fall in vascular resistance was linearly related to log VIP output after total muscarinic blockade. Intracarotid infusions of synthetic VIP produced dose-dependent falls in submandibular vascular resistance, together with a corresponding increase in submandibular blood flow. It is concluded tha...

  • submandibular secretory and vascular responses to stimulation of the Parasympathetic Innervation in anesthetized cats
    Journal of Applied Physiology, 2000
    Co-Authors: K Rourke, A V Edwards
    Abstract:

    Submandibular secretory responses to stimulation of the Parasympathetic chorda-lingual nerve in anaesthetized cats have been investigated before, during, and after intracarotid infusion of endothelin-1 (ET-1), which reduced blood flow through the gland by 64 ± 7%. Stimulation at different frequencies (2, 4, 8, and 16 Hz) evoked a frequency-dependent increase in the flow of submandibular saliva, sodium concentration and output, and output of both potassium and protein. The reduction in submandibular blood flow, which occurred in response to the infusion of ET-1, was associated with a decreased flow of saliva and a diminished output of both sodium and protein. The flow of saliva was linearly related to submandibular blood flow both in the presence and absence of ET-1. It is concluded that submandibular secretory responses to electrical stimulation of the Parasympathetic Innervation can be significantly attenuated by reducing the blood flow through the gland by ET-1 infusion, just as it is when the blood flow is reduced by hypotension.

  • submandibular responses to stimulation of the Parasympathetic Innervation in bursts in the anaesthetized ferret
    The Journal of Physiology, 1990
    Co-Authors: G Tobin, J Ekstrom, A V Edwards
    Abstract:

    1. Submandibular salivary and vascular responses to different patterns of stimulation of the Parasympathetic Innervation have been investigated in anaesthetized ferrets in the presence and absence of atropine. 2. At low stimulus frequencies likely to fall within the physiological range (0.5-2.0 Hz continuously; 5.0-20.0 Hz in 1 s bursts at 10 s intervals) secretion of fluid and protein were both potentiated by the bursting pattern of stimulation and the latency of the secretory response was reduced. Over a somewhat lower range (0.5-1.0 Hz continuously; 5.0-10.0 Hz in bursts) the submandibular vascular response was also significantly potentiated by employing this intermittent pattern of stimulation. Above these frequency ranges no such potentiation occurred. 3. Pre-treatment with atropine (2.0 mg kg-1) blocked the submandibular secretory responses to stimulation of the chorda-lingual nerve at these low frequencies and the residual responses at higher frequencies were not significantly affected by changing the pattern of stimulation. The vascular response was somewhat reduced after atropine but that which persisted was enhanced by stimulating in bursts. 4. It is concluded that the release of some transmitter from postganglionic terminals in the submandibular gland of the ferret must be potentiated by the arrival of action potentials at short intervals and possible mechanisms are considered.

D Rangaraj - One of the best experts on this subject based on the ideXlab platform.

  • transient activation of hedgehog pathway rescued irradiation induced hyposalivation by preserving salivary stem progenitor cells and Parasympathetic Innervation
    Clinical Cancer Research, 2014
    Co-Authors: Zhenhua Yang, Qingguo Zhao, Lei Shangguan, Xinyu Ti, Yanqiu Zhao, D Rangaraj
    Abstract:

    Purpose: To examine the effects and mechanisms of transient activation of the Hedgehog pathway on rescuing radiotherapy-induced hyposalivation in survivors of head and neck cancer. Experimental Design: Mouse salivary glands and cultured human salivary epithelial cells were irradiated by a single 15-Gy dose. The Hedgehog pathway was transiently activated in mouse salivary glands, by briefly overexpressing the Sonic hedgehog (Shh) transgene or administrating smoothened agonist, and in human salivary epithelial cells, by infecting with adenovirus encoding Gli1. The activity of Hedgehog signaling was examined by the expression of the Ptch1-lacZ reporter and endogenous Hedgehog target genes. The salivary flow rate was measured following pilocarpine stimulation. Salivary stem/progenitor cells (SSPC), Parasympathetic Innervation, and expression of related genes were examined by flow cytometry, salisphere assay, immunohistochemistry, quantitative reverse transcription PCR, Western blotting, and ELISA. Results: Irradiation does not activate Hedgehog signaling in mouse salivary glands. Transient Shh overexpression activated the Hedgehog pathway in ductal epithelia and, after irradiation, rescued salivary function in male mice, which is related with preservation of functional SSPCs and Parasympathetic Innervation. The preservation of SSPCs was likely mediated by the rescue of signaling activities of the Bmi1 and Chrm1–HB-EGF pathways. The preservation of Parasympathetic Innervation was associated with the rescue of the expression of neurotrophic factors such as Bdnf and Nrtn. The expression of genes related with maintenance of SSPCs and Parasympathetic Innervation in female salivary glands and cultured human salivary epithelial cells was similarly affected by irradiation and transient Hedgehog activation. Conclusions: These findings suggest that transient activation of the Hedgehog pathway has the potential to restore salivary gland function after irradiation-induced dysfunction. Clin Cancer Res; 20(1); 140–50. ©2013 AACR .

  • Transient Activation of Hedgehog Pathway Rescued Irradiation-Induced Hyposalivation by Preserving Salivary Stem/Progenitor Cells and Parasympathetic Innervation
    Clinical Cancer Research, 2013
    Co-Authors: Zhenhua Yang, Qingguo Zhao, Lei Shangguan, Xinyu Ti, Yanqiu Zhao, D Rangaraj
    Abstract:

    Purpose: To examine the effects and mechanisms of transient activation of the Hedgehog pathway on rescuing radiotherapy-induced hyposalivation in survivors of head and neck cancer. Experimental Design: Mouse salivary glands and cultured human salivary epithelial cells were irradiated by a single 15-Gy dose. The Hedgehog pathway was transiently activated in mouse salivary glands, by briefly overexpressing the Sonic hedgehog (Shh) transgene or administrating smoothened agonist, and in human salivary epithelial cells, by infecting with adenovirus encoding Gli1. The activity of Hedgehog signaling was examined by the expression of the Ptch1-lacZ reporter and endogenous Hedgehog target genes. The salivary flow rate was measured following pilocarpine stimulation. Salivary stem/progenitor cells (SSPC), Parasympathetic Innervation, and expression of related genes were examined by flow cytometry, salisphere assay, immunohistochemistry, quantitative reverse transcription PCR, Western blotting, and ELISA. Results: Irradiation does not activate Hedgehog signaling in mouse salivary glands. Transient Shh overexpression activated the Hedgehog pathway in ductal epithelia and, after irradiation, rescued salivary function in male mice, which is related with preservation of functional SSPCs and Parasympathetic Innervation. The preservation of SSPCs was likely mediated by the rescue of signaling activities of the Bmi1 and Chrm1–HB-EGF pathways. The preservation of Parasympathetic Innervation was associated with the rescue of the expression of neurotrophic factors such as Bdnf and Nrtn. The expression of genes related with maintenance of SSPCs and Parasympathetic Innervation in female salivary glands and cultured human salivary epithelial cells was similarly affected by irradiation and transient Hedgehog activation. Conclusions: These findings suggest that transient activation of the Hedgehog pathway has the potential to restore salivary gland function after irradiation-induced dysfunction. Clin Cancer Res; 20(1); 140–50. ©2013 AACR .

Patrick C N Rensen - One of the best experts on this subject based on the ideXlab platform.

R M Mcallen - One of the best experts on this subject based on the ideXlab platform.

Zhenhua Yang - One of the best experts on this subject based on the ideXlab platform.

  • transient activation of hedgehog pathway rescued irradiation induced hyposalivation by preserving salivary stem progenitor cells and Parasympathetic Innervation
    Clinical Cancer Research, 2014
    Co-Authors: Zhenhua Yang, Qingguo Zhao, Lei Shangguan, Xinyu Ti, Yanqiu Zhao, D Rangaraj
    Abstract:

    Purpose: To examine the effects and mechanisms of transient activation of the Hedgehog pathway on rescuing radiotherapy-induced hyposalivation in survivors of head and neck cancer. Experimental Design: Mouse salivary glands and cultured human salivary epithelial cells were irradiated by a single 15-Gy dose. The Hedgehog pathway was transiently activated in mouse salivary glands, by briefly overexpressing the Sonic hedgehog (Shh) transgene or administrating smoothened agonist, and in human salivary epithelial cells, by infecting with adenovirus encoding Gli1. The activity of Hedgehog signaling was examined by the expression of the Ptch1-lacZ reporter and endogenous Hedgehog target genes. The salivary flow rate was measured following pilocarpine stimulation. Salivary stem/progenitor cells (SSPC), Parasympathetic Innervation, and expression of related genes were examined by flow cytometry, salisphere assay, immunohistochemistry, quantitative reverse transcription PCR, Western blotting, and ELISA. Results: Irradiation does not activate Hedgehog signaling in mouse salivary glands. Transient Shh overexpression activated the Hedgehog pathway in ductal epithelia and, after irradiation, rescued salivary function in male mice, which is related with preservation of functional SSPCs and Parasympathetic Innervation. The preservation of SSPCs was likely mediated by the rescue of signaling activities of the Bmi1 and Chrm1–HB-EGF pathways. The preservation of Parasympathetic Innervation was associated with the rescue of the expression of neurotrophic factors such as Bdnf and Nrtn. The expression of genes related with maintenance of SSPCs and Parasympathetic Innervation in female salivary glands and cultured human salivary epithelial cells was similarly affected by irradiation and transient Hedgehog activation. Conclusions: These findings suggest that transient activation of the Hedgehog pathway has the potential to restore salivary gland function after irradiation-induced dysfunction. Clin Cancer Res; 20(1); 140–50. ©2013 AACR .

  • Transient Activation of Hedgehog Pathway Rescued Irradiation-Induced Hyposalivation by Preserving Salivary Stem/Progenitor Cells and Parasympathetic Innervation
    Clinical Cancer Research, 2013
    Co-Authors: Zhenhua Yang, Qingguo Zhao, Lei Shangguan, Xinyu Ti, Yanqiu Zhao, D Rangaraj
    Abstract:

    Purpose: To examine the effects and mechanisms of transient activation of the Hedgehog pathway on rescuing radiotherapy-induced hyposalivation in survivors of head and neck cancer. Experimental Design: Mouse salivary glands and cultured human salivary epithelial cells were irradiated by a single 15-Gy dose. The Hedgehog pathway was transiently activated in mouse salivary glands, by briefly overexpressing the Sonic hedgehog (Shh) transgene or administrating smoothened agonist, and in human salivary epithelial cells, by infecting with adenovirus encoding Gli1. The activity of Hedgehog signaling was examined by the expression of the Ptch1-lacZ reporter and endogenous Hedgehog target genes. The salivary flow rate was measured following pilocarpine stimulation. Salivary stem/progenitor cells (SSPC), Parasympathetic Innervation, and expression of related genes were examined by flow cytometry, salisphere assay, immunohistochemistry, quantitative reverse transcription PCR, Western blotting, and ELISA. Results: Irradiation does not activate Hedgehog signaling in mouse salivary glands. Transient Shh overexpression activated the Hedgehog pathway in ductal epithelia and, after irradiation, rescued salivary function in male mice, which is related with preservation of functional SSPCs and Parasympathetic Innervation. The preservation of SSPCs was likely mediated by the rescue of signaling activities of the Bmi1 and Chrm1–HB-EGF pathways. The preservation of Parasympathetic Innervation was associated with the rescue of the expression of neurotrophic factors such as Bdnf and Nrtn. The expression of genes related with maintenance of SSPCs and Parasympathetic Innervation in female salivary glands and cultured human salivary epithelial cells was similarly affected by irradiation and transient Hedgehog activation. Conclusions: These findings suggest that transient activation of the Hedgehog pathway has the potential to restore salivary gland function after irradiation-induced dysfunction. Clin Cancer Res; 20(1); 140–50. ©2013 AACR .