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Article: Autonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogs

TitleAutonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogs
Authors
Keywordsα- and β-adrenergic mechanisms
Arteriovenous anastomoses
Muscarinic and peptidergic receptors
Parasympathetic salivation
Issue Date1998
PublisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/
Citation
American Journal Of Physiology - Gastrointestinal And Liver Physiology, 1998, v. 275 n. 2 38-2, p. G331-G341 How to Cite?
AbstractIn dogs anesthetized with pentobarbital sodium, hilar venous pressure (P(hv)) and secretion were measured from the submandibular gland receiving spontaneous blood flow or vascular perfusion at the normal resting flow rate. Parasympathetic nerve stimulation and ACh-induced secretion increased P(hv) and its pulse pressure; P(hv) also showed an obvious arterial (or perfusion pressure)-like waveform. Vasoactive intestinal polypeptide (VIP) exerted similar effects on P(hv) but produced negligible secretion. Sympathetic nerve stimulation, phenylephrine, and clonidine did not induce secretion and had no significant action on P(hv), whereas isoproterenol provoked secretion and changed P(hv) as with parasympathetic stimulation. Background or superimposed sympathetic nerve stimulation reduced the parasympathetic nerve-induced responses; the sympathetic inhibition was abolished by phentolamine and yohimbine but not by prazosin and propranolol. The results suggest a direct relationship between P(hv) and secretion during parasympathetic salivation: The elevation in P(hv) was primarily independent of the concurrent blood flow response, mediated via muscarinic and peptidergic mechanisms, and related to an opening of arteriovenous anastomoses. Sympathetic inhibition of parasympathetic salivation may be related to prevention of an increased P(hv) exerted primarily via the α2-adrenergic mechanism.
Persistent Identifierhttp://hdl.handle.net/10722/49298
ISSN
2015 Impact Factor: 3.297
2015 SCImago Journal Rankings: 1.936
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLung, MAen_HK
dc.date.accessioned2008-06-12T06:38:49Z-
dc.date.available2008-06-12T06:38:49Z-
dc.date.issued1998en_HK
dc.identifier.citationAmerican Journal Of Physiology - Gastrointestinal And Liver Physiology, 1998, v. 275 n. 2 38-2, p. G331-G341en_HK
dc.identifier.issn0193-1857en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49298-
dc.description.abstractIn dogs anesthetized with pentobarbital sodium, hilar venous pressure (P(hv)) and secretion were measured from the submandibular gland receiving spontaneous blood flow or vascular perfusion at the normal resting flow rate. Parasympathetic nerve stimulation and ACh-induced secretion increased P(hv) and its pulse pressure; P(hv) also showed an obvious arterial (or perfusion pressure)-like waveform. Vasoactive intestinal polypeptide (VIP) exerted similar effects on P(hv) but produced negligible secretion. Sympathetic nerve stimulation, phenylephrine, and clonidine did not induce secretion and had no significant action on P(hv), whereas isoproterenol provoked secretion and changed P(hv) as with parasympathetic stimulation. Background or superimposed sympathetic nerve stimulation reduced the parasympathetic nerve-induced responses; the sympathetic inhibition was abolished by phentolamine and yohimbine but not by prazosin and propranolol. The results suggest a direct relationship between P(hv) and secretion during parasympathetic salivation: The elevation in P(hv) was primarily independent of the concurrent blood flow response, mediated via muscarinic and peptidergic mechanisms, and related to an opening of arteriovenous anastomoses. Sympathetic inhibition of parasympathetic salivation may be related to prevention of an increased P(hv) exerted primarily via the α2-adrenergic mechanism.en_HK
dc.format.extent418 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherAmerican Physiological Society. The Journal's web site is located at http://intl-ajpgi.physiology.org/en_HK
dc.relation.ispartofAmerican Journal of Physiology - Gastrointestinal and Liver Physiologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectα- and β-adrenergic mechanismsen_HK
dc.subjectArteriovenous anastomosesen_HK
dc.subjectMuscarinic and peptidergic receptorsen_HK
dc.subjectParasympathetic salivationen_HK
dc.titleAutonomic nervous control of venous pressure and secretion in submandibular gland of anesthetized dogsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0193-1857&volume=275&issue=2&spage=G331&epage=G341&date=1998&atitle=Autonomic+nervous+control+of+venous+pressure+and+secretion+in+submandibular+gland+of+anesthetized+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.pmid9688661-
dc.identifier.scopuseid_2-s2.0-0031867636en_HK
dc.identifier.hkuros37930-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0031867636&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume275en_HK
dc.identifier.issue2 38-2en_HK
dc.identifier.spageG331en_HK
dc.identifier.epageG341en_HK
dc.identifier.isiWOS:000075289300020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLung, MA=7006411781en_HK

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