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- Publisher Website: 10.1111/j.1476-5381.1994.tb13087.x
- Scopus: eid_2-s2.0-0028275527
- PMID: 8075858
- WOS: WOS:A1994NN63600013
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Article: Mechanisms of sympathetic enhancement and inhibition of parasympathetically induced salivary secretion in anaesthetized dogs
Title | Mechanisms of sympathetic enhancement and inhibition of parasympathetically induced salivary secretion in anaesthetized dogs |
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Authors | |
Keywords | enhancement is via α1‐adrenoceptors whereas inhibition is via α2‐adrenoceptors. Parasympathetic salivation postsynaptic α1‐adrenoceptors postsynaptic α2‐adrenoceptors sympathetic enhancement of salivary flow sympathetic inhibition of salivary flow |
Issue Date | 1994 |
Publisher | John Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1 |
Citation | British Journal Of Pharmacology, 1994, v. 112 n. 2, p. 411-416 How to Cite? |
Abstract | The effects of superimposed and continuous sympathetic nerve stimulation on submandibular parasympathetic salivation were investigated in anaesthetized dogs. Superimposed sympathetic nerve stimulation (1-2 min) initially enhanced and later inhibited salivary secretion induced by parasympathetic nerve stimulation (2-8 Hz) in glands with uncontrolled blood supply or constant-flow vascular perfusion. Propranolol 0.005 mg kg-1, i.a.) did not affect the diphasic sympathetic action whereas phentolamine (0.1 mg kg-1, i.a.) abolished it. Prazosin (0.025 mg kg-1, i.a.) greatly lessened the initial enhancement while yohimbine (0.025 mg kg-1, i.a.) alleviated the late inhibition. Salivary secretion, induced by parasympathetic nerve stimulation (4 Hz) or acetylcholine infusion (10 μg kg-1 min-1, i.a.), was abolished by atropine (0.05 mg kg-1, i.a.), increased by phenylephrine infusion (0.25 μg kg-1 min-1, i.a.) and depressed by clonidine infusion (0.75 μg kg-1 min-1, i.a.). Hexamethionium (12.5 mg kg-1, i.a.) abolished the nerve-induced secretion but had no effect on the acetylcholine-induced secretion. Continuous background sympathetic nerve stimulation decreased parasympathetic nerve-induced salivary secretion in glands with uncontrolled blood supply or constant-flow vascular perfusion. These results show that parasympathetic salivation can be modified by the sympathetic system at the postsynaptic level; enhancement is via α1-adrenoceptors whereas inhibition is via a2-adrenoceptors. |
Persistent Identifier | http://hdl.handle.net/10722/171607 |
ISSN | 2023 Impact Factor: 6.8 2023 SCImago Journal Rankings: 2.119 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Lung, MA | en_US |
dc.date.accessioned | 2012-10-30T06:15:56Z | - |
dc.date.available | 2012-10-30T06:15:56Z | - |
dc.date.issued | 1994 | en_US |
dc.identifier.citation | British Journal Of Pharmacology, 1994, v. 112 n. 2, p. 411-416 | en_US |
dc.identifier.issn | 0007-1188 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171607 | - |
dc.description.abstract | The effects of superimposed and continuous sympathetic nerve stimulation on submandibular parasympathetic salivation were investigated in anaesthetized dogs. Superimposed sympathetic nerve stimulation (1-2 min) initially enhanced and later inhibited salivary secretion induced by parasympathetic nerve stimulation (2-8 Hz) in glands with uncontrolled blood supply or constant-flow vascular perfusion. Propranolol 0.005 mg kg-1, i.a.) did not affect the diphasic sympathetic action whereas phentolamine (0.1 mg kg-1, i.a.) abolished it. Prazosin (0.025 mg kg-1, i.a.) greatly lessened the initial enhancement while yohimbine (0.025 mg kg-1, i.a.) alleviated the late inhibition. Salivary secretion, induced by parasympathetic nerve stimulation (4 Hz) or acetylcholine infusion (10 μg kg-1 min-1, i.a.), was abolished by atropine (0.05 mg kg-1, i.a.), increased by phenylephrine infusion (0.25 μg kg-1 min-1, i.a.) and depressed by clonidine infusion (0.75 μg kg-1 min-1, i.a.). Hexamethionium (12.5 mg kg-1, i.a.) abolished the nerve-induced secretion but had no effect on the acetylcholine-induced secretion. Continuous background sympathetic nerve stimulation decreased parasympathetic nerve-induced salivary secretion in glands with uncontrolled blood supply or constant-flow vascular perfusion. These results show that parasympathetic salivation can be modified by the sympathetic system at the postsynaptic level; enhancement is via α1-adrenoceptors whereas inhibition is via a2-adrenoceptors. | en_US |
dc.language | eng | en_US |
dc.publisher | John Wiley & Sons Ltd. The Journal's web site is located at http://www.wiley.com/bw/journal.asp?ref=0007-1188&site=1 | en_US |
dc.relation.ispartof | British Journal of Pharmacology | en_US |
dc.subject | enhancement is via α1‐adrenoceptors whereas inhibition is via α2‐adrenoceptors. | - |
dc.subject | Parasympathetic salivation | - |
dc.subject | postsynaptic α1‐adrenoceptors | - |
dc.subject | postsynaptic α2‐adrenoceptors | - |
dc.subject | sympathetic enhancement of salivary flow | - |
dc.subject | sympathetic inhibition of salivary flow | - |
dc.subject.mesh | Adrenergic Alpha-1 Receptor Antagonists | en_US |
dc.subject.mesh | Adrenergic Alpha-2 Receptor Antagonists | en_US |
dc.subject.mesh | Anesthesia | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Blood Pressure - Drug Effects | en_US |
dc.subject.mesh | Dogs | en_US |
dc.subject.mesh | Electric Stimulation | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Male | en_US |
dc.subject.mesh | Parasympathetic Nervous System - Drug Effects - Physiology | en_US |
dc.subject.mesh | Regional Blood Flow - Drug Effects | en_US |
dc.subject.mesh | Salivation - Drug Effects - Physiology | en_US |
dc.subject.mesh | Submandibular Gland - Blood Supply - Drug Effects - Secretion | en_US |
dc.subject.mesh | Sympathetic Nervous System - Drug Effects - Physiology | en_US |
dc.title | Mechanisms of sympathetic enhancement and inhibition of parasympathetically induced salivary secretion in anaesthetized dogs | en_US |
dc.type | Article | en_US |
dc.identifier.email | Lung, MA:makylung@hkucc.hku.hk | en_US |
dc.identifier.authority | Lung, MA=rp00319 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.doi | 10.1111/j.1476-5381.1994.tb13087.x | - |
dc.identifier.pmid | 8075858 | - |
dc.identifier.scopus | eid_2-s2.0-0028275527 | en_US |
dc.identifier.volume | 112 | en_US |
dc.identifier.issue | 2 | en_US |
dc.identifier.spage | 411 | en_US |
dc.identifier.epage | 416 | en_US |
dc.identifier.isi | WOS:A1994NN63600013 | - |
dc.publisher.place | United Kingdom | en_US |
dc.identifier.scopusauthorid | Lung, MA=7006411781 | en_US |
dc.identifier.issnl | 0007-1188 | - |