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Article: Relationship of rostral ventrolateral medullary neurons and angiotensin in the central control of blood pressure

TitleRelationship of rostral ventrolateral medullary neurons and angiotensin in the central control of blood pressure
Authors
KeywordsAngiotensin II
Arterial pressure
Cardiovascular neurons
Discharge units, single and double
Hypertensive rat, spontaneously
Rostral ventrolateral medulla
Issue Date1995
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
Biological Signals, 1995, v. 4 n. 3, p. 133-141 How to Cite?
AbstractThe rostral ventrolateral medulla (RVL) in the medulla oblongata contains a group of vasomotor neurons that regulate the level of arterial blood pressure. That these spinal-projecting neurons were spontaneously active, cardiac-locked and barosensitive further underlies their important role in generating a tonic sympathoexcitatory outflow. In pentobarbital anesthetized spontaneously hypertensive rats (SHR), the electrophysiological behaviours of these sympathoexcitatory cardiovascular neurons were significantly different from those of normotensive Wistar Kyoto rats (WKY). In SHR, there was an equal occurrence of slow-conducting single discharge units and fast-conducting double discharge units while the vast majority of RVL neurons was single discharge units in WKY. Further, the single discharge units of SHR had a higher firing rate and a more regular discharge pattern than those in WKY. The activity of a subpopulation of these RVL cardiovascular neurons was excited by iontophoretic application of angiotensin II, with the magnitude and duration of the excitation greater in SHR than in WKY. Besides, microinjection of [Sar1, Ile8]-angiotensin II, an angiotensin II antagonist, to RVL caused a greater decrease in the firing rate of a subpopulation of RVL cardiovascular neurons in SHR than in WKY. In both types of rats, the neuronal responses were significantly greater in double discharge units than in single discharge units. This was followed by a subsequent depressor response which was significantly greater in SHR than in WKY. These observations demonstrate that in SHR the altered spontaneous electrophysiological property of sympathoexcitatory neurons in the RVL and their augmented sensitivity to the tonic influence of brain angiotensin may contribute to the manifestation of hypertension in this strain of rats.
Persistent Identifierhttp://hdl.handle.net/10722/81228
ISSN
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, YSen_HK
dc.contributor.authorWong, TMen_HK
dc.date.accessioned2010-09-06T08:15:16Z-
dc.date.available2010-09-06T08:15:16Z-
dc.date.issued1995en_HK
dc.identifier.citationBiological Signals, 1995, v. 4 n. 3, p. 133-141en_HK
dc.identifier.issn1016-0922en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81228-
dc.description.abstractThe rostral ventrolateral medulla (RVL) in the medulla oblongata contains a group of vasomotor neurons that regulate the level of arterial blood pressure. That these spinal-projecting neurons were spontaneously active, cardiac-locked and barosensitive further underlies their important role in generating a tonic sympathoexcitatory outflow. In pentobarbital anesthetized spontaneously hypertensive rats (SHR), the electrophysiological behaviours of these sympathoexcitatory cardiovascular neurons were significantly different from those of normotensive Wistar Kyoto rats (WKY). In SHR, there was an equal occurrence of slow-conducting single discharge units and fast-conducting double discharge units while the vast majority of RVL neurons was single discharge units in WKY. Further, the single discharge units of SHR had a higher firing rate and a more regular discharge pattern than those in WKY. The activity of a subpopulation of these RVL cardiovascular neurons was excited by iontophoretic application of angiotensin II, with the magnitude and duration of the excitation greater in SHR than in WKY. Besides, microinjection of [Sar1, Ile8]-angiotensin II, an angiotensin II antagonist, to RVL caused a greater decrease in the firing rate of a subpopulation of RVL cardiovascular neurons in SHR than in WKY. In both types of rats, the neuronal responses were significantly greater in double discharge units than in single discharge units. This was followed by a subsequent depressor response which was significantly greater in SHR than in WKY. These observations demonstrate that in SHR the altered spontaneous electrophysiological property of sympathoexcitatory neurons in the RVL and their augmented sensitivity to the tonic influence of brain angiotensin may contribute to the manifestation of hypertension in this strain of rats.en_HK
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofBiological Signalsen_HK
dc.rightsBiological Signals. Copyright © S Karger AG.en_HK
dc.subjectAngiotensin IIen_HK
dc.subjectArterial pressureen_HK
dc.subjectCardiovascular neuronsen_HK
dc.subjectDischarge units, single and doubleen_HK
dc.subjectHypertensive rat, spontaneouslyen_HK
dc.subjectRostral ventrolateral medullaen_HK
dc.titleRelationship of rostral ventrolateral medullary neurons and angiotensin in the central control of blood pressureen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1016-0922&volume=4&spage=133&epage=141&date=1995&atitle=Relationship+of+rostral+ventrolateral+medullary+neurons+and+angiotensin+in+the+central+control+of+blood+pressureen_HK
dc.identifier.emailChan, YS: yschan@hkucc.hku.hken_HK
dc.identifier.authorityChan, YS=rp00318en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid8750939-
dc.identifier.scopuseid_2-s2.0-84939665188en_HK
dc.identifier.hkuros12826en_HK
dc.identifier.volume4en_HK
dc.identifier.issue3en_HK
dc.identifier.spage133en_HK
dc.identifier.epage141en_HK
dc.identifier.isiWOS:A1995TN13500004-
dc.publisher.placeSwitzerlanden_HK
dc.identifier.scopusauthoridChan, YS=7403676627en_HK
dc.identifier.scopusauthoridWong, TM=7403531434en_HK
dc.identifier.issnl1016-0922-

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