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Article: Autonomic nervous control of myoepithelial cells and secretion in submandibular gland of anaesthetized dogs

TitleAutonomic nervous control of myoepithelial cells and secretion in submandibular gland of anaesthetized dogs
Authors
Issue Date2003
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751
Citation
Journal Of Physiology, 2003, v. 546 n. 3, p. 837-850 How to Cite?
AbstractIn dog submandibular gland, the activity of myoepithelial cells was assessed by simultaneous measurement of intraductal pressure (Pdu) and subcapsular pressure (Pca) using catheter-tip pressure transducers; their resting values were 2.5 ± 0.21 and 3.0 ± 0.19 mmHg, respectively (n = 40). Retrograde infusion of saliva (collected from preceding parasympathetic nerve stimulation) increased Pdu (coefficient of 50 mmHg ml-1 for rates < 1 ml min-1 and 85 mmHg ml-1 for higher rates) and Pca (coefficient of 0.47 mmHg ml-1 for all rates). Blood flow changes did not affect Pdu but increased Pca (coefficient of 0.04 mmHg ml-1). Parasympathetic nerve stimulation increased Pdu but decreased Pca abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for Pdu and Pca on salivary secretion to parasympathetic nerve stimulation in glands with spontaneous blood flow (5.3 × 106-3 and 4.87 × 10-2 ml min-1 g-1 mmHg-1) were close to their values in glands with constant-flow vascular perfusion (4.9 × 10-3 and 3.68 × 10-2 ml min-1 g-1 mmHg-1). The finding that Pca fell despite concomitant increased blood flow suggests contraction of myoepithelial cells. Additional ductal occlusion further increased Pdu and enhanced the fall in Pca, suggesting that the myoepithelial cells can contract when distended. Atropine blocked salivary secretion and responses of Pdu and Pca; to parasympathetic nerve stimulation. ACh elicited responses similar to that of parasympathetic nerve stimulation. VIP caused very scanty salivary secretion and gradual slight increases in Pdu and Pca; the change in Pca was abolished in glands with constant-flow vascular perfusion. Hence, contraction of myoepithelial cells to parasympathetic nerve stimulation is via muscarinic receptors. Sympathetic nerve stimulation increased Pdu and decreased Pca abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for Pdu and Pca on salivary secretion to sympathetic nerve stimulation in glands with spontaneous blood flow (3.0 × 10-3 and 3.2 × 10-3 ml min-1 g-1 mmHg-1) were similar to their values in glands with constant-flow vascular perfusion (3.2 × 10-3 and 3.1 × 10-3 ml min-1 g-1 mmHg-1). The finding that Pca fell even in glands with constant-flow vascular perfusion suggests contraction of myoepithelial cells. Superimposed sympathetic nerve stimulation immediately enhanced the pressure changes and secretory response to parasympathetic nerve stimulation, indicating that the two autonomic nerves act synergistically to evoke myoepithelial cell contraction. Phentolamine and prazosin but not propranolol and yohimbine blocked the sympathetic enhancement. The finding that phenylephrine, but not clonidine and isoproterenol, abruptly decreased Pca in glands with constant-flow vascular perfusion suggests that the sympathetic activation of myoepithelial cells is via the α1-adrenoceptors.
Persistent Identifierhttp://hdl.handle.net/10722/49306
ISSN
2015 Impact Factor: 4.731
2015 SCImago Journal Rankings: 2.670
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLung, MAen_HK
dc.date.accessioned2008-06-12T06:38:58Z-
dc.date.available2008-06-12T06:38:58Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Physiology, 2003, v. 546 n. 3, p. 837-850en_HK
dc.identifier.issn0022-3751en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49306-
dc.description.abstractIn dog submandibular gland, the activity of myoepithelial cells was assessed by simultaneous measurement of intraductal pressure (Pdu) and subcapsular pressure (Pca) using catheter-tip pressure transducers; their resting values were 2.5 ± 0.21 and 3.0 ± 0.19 mmHg, respectively (n = 40). Retrograde infusion of saliva (collected from preceding parasympathetic nerve stimulation) increased Pdu (coefficient of 50 mmHg ml-1 for rates < 1 ml min-1 and 85 mmHg ml-1 for higher rates) and Pca (coefficient of 0.47 mmHg ml-1 for all rates). Blood flow changes did not affect Pdu but increased Pca (coefficient of 0.04 mmHg ml-1). Parasympathetic nerve stimulation increased Pdu but decreased Pca abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for Pdu and Pca on salivary secretion to parasympathetic nerve stimulation in glands with spontaneous blood flow (5.3 × 106-3 and 4.87 × 10-2 ml min-1 g-1 mmHg-1) were close to their values in glands with constant-flow vascular perfusion (4.9 × 10-3 and 3.68 × 10-2 ml min-1 g-1 mmHg-1). The finding that Pca fell despite concomitant increased blood flow suggests contraction of myoepithelial cells. Additional ductal occlusion further increased Pdu and enhanced the fall in Pca, suggesting that the myoepithelial cells can contract when distended. Atropine blocked salivary secretion and responses of Pdu and Pca; to parasympathetic nerve stimulation. ACh elicited responses similar to that of parasympathetic nerve stimulation. VIP caused very scanty salivary secretion and gradual slight increases in Pdu and Pca; the change in Pca was abolished in glands with constant-flow vascular perfusion. Hence, contraction of myoepithelial cells to parasympathetic nerve stimulation is via muscarinic receptors. Sympathetic nerve stimulation increased Pdu and decreased Pca abruptly; the response threshold was 0.1 Hz, with maximal responses at 16 Hz. The coefficients for Pdu and Pca on salivary secretion to sympathetic nerve stimulation in glands with spontaneous blood flow (3.0 × 10-3 and 3.2 × 10-3 ml min-1 g-1 mmHg-1) were similar to their values in glands with constant-flow vascular perfusion (3.2 × 10-3 and 3.1 × 10-3 ml min-1 g-1 mmHg-1). The finding that Pca fell even in glands with constant-flow vascular perfusion suggests contraction of myoepithelial cells. Superimposed sympathetic nerve stimulation immediately enhanced the pressure changes and secretory response to parasympathetic nerve stimulation, indicating that the two autonomic nerves act synergistically to evoke myoepithelial cell contraction. Phentolamine and prazosin but not propranolol and yohimbine blocked the sympathetic enhancement. The finding that phenylephrine, but not clonidine and isoproterenol, abruptly decreased Pca in glands with constant-flow vascular perfusion suggests that the sympathetic activation of myoepithelial cells is via the α1-adrenoceptors.en_HK
dc.format.extent420 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0022-3751en_HK
dc.relation.ispartofJournal of Physiologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsThe Journal of Physiology. Copyright © Blackwell Publishing Ltd.en_HK
dc.rightsThe definitive version is available at www.blackwell-synergy.comen_HK
dc.subject.meshAutonomic Nervous System - physiologyen_HK
dc.subject.meshMyocytes, Smooth Muscle - metabolismen_HK
dc.subject.meshSubmandibular Gland - blood supply - cytology - innervation - secretionen_HK
dc.subject.meshSympathetic Nervous System - physiologyen_HK
dc.subject.meshEpithelial Cells - metabolismen_HK
dc.titleAutonomic nervous control of myoepithelial cells and secretion in submandibular gland of anaesthetized dogsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-3751&volume=546&issue=3&spage=837&epage=850&date=2003&atitle=Autonomic+nervous+control+of+myoepithelial+cells+and+secretion+in+submandibular+gland+of+anaesthetized+dogsen_HK
dc.identifier.emailLung, MA: makylung@hkucc.hku.hken_HK
dc.identifier.authorityLung, MA=rp00319en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1113/jphysiol.2002.029686en_HK
dc.identifier.pmid12563008-
dc.identifier.pmcidPMC3204443-
dc.identifier.scopuseid_2-s2.0-0037320712en_HK
dc.identifier.hkuros81675-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037320712&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume546en_HK
dc.identifier.issue3en_HK
dc.identifier.spage837en_HK
dc.identifier.epage850en_HK
dc.identifier.isiWOS:000183570000018-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLung, MA=7006411781en_HK

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