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Article: Adrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats

TitleAdrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive rats
Authors
Issue Date1981
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1981, v. 3 n. 1, p. 93-103 How to Cite?
AbstractThe goal of this study was to compare adrenergic neurotransmission in isolated vascular smooth muscle from spontaneously hypertensive (SHR) and normotensive rats. Tail arteries, excised from adult SHR and normotensive rats, were cut helically into strips that were mounted in organ chambers between two platinum wire electrodes; isometric contractions were recorded. Vascular responsiveness was determined before and after acute denervation with 6-hydroxydopamine or before and after treatment with phentolamine. Release or displacement of endogenous norepinephrine was obtained with electrical stimulation, tyramine, and potassium. The sensitivity to exogenous norepinephrine of innervated vessels was similar for SHR and normotensive rats. Denervation produced a significant shift to the left in the concentration-response curve to norepinephrine only in SHR vessels. Contractile responses to electrical stimulation, tyramine, and potassium were similar in both groups before denervation. Contractile responses to potassium-free solution were greater in SHR than in normotensive vessels. Following denervation, the SHR and normotensive vessels responded similarly to these latter interventions. Blockade of alpha-adrenoceptors with phentolamine reduced contractile responses to all agents in innervated and denervated vessels. Cocaine caused a slowing of the relaxation following contraction induced by electrical stimulation in both SHR and normotensive vessels. The relaxation of SHR vessels was less affected by cocaine than in normotensive vessels. The tissue content of norepinephrine was similar in SHR and normotensive arterial strips. In arterial strips from SHR the uptake of 3H-norepinephrine was significantly larger than in those from normotensive rats. The results suggest that the reactivity of innervated blood vessels to norepinephrine is similar in SHR and normotensive rats. Important differences in sensitivity to norepinephrine in hypertensive vessels are unmasked when the relationship between the vascular smooth muscle cell and the adrenergic nerve terminal is altered. Apparently, the adrenergic nerve terminals in hypertensive blood vessel can modulate the junctional concentration of norepinephrine so that the contractile response to this agent is similar to that in normotensive blood vessels.
Persistent Identifierhttp://hdl.handle.net/10722/170627
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWebb, RCen_US
dc.contributor.authorVanhoutte, PMen_US
dc.contributor.authorBohr, DFen_US
dc.date.accessioned2012-10-30T06:10:11Z-
dc.date.available2012-10-30T06:10:11Z-
dc.date.issued1981en_US
dc.identifier.citationHypertension, 1981, v. 3 n. 1, p. 93-103en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170627-
dc.description.abstractThe goal of this study was to compare adrenergic neurotransmission in isolated vascular smooth muscle from spontaneously hypertensive (SHR) and normotensive rats. Tail arteries, excised from adult SHR and normotensive rats, were cut helically into strips that were mounted in organ chambers between two platinum wire electrodes; isometric contractions were recorded. Vascular responsiveness was determined before and after acute denervation with 6-hydroxydopamine or before and after treatment with phentolamine. Release or displacement of endogenous norepinephrine was obtained with electrical stimulation, tyramine, and potassium. The sensitivity to exogenous norepinephrine of innervated vessels was similar for SHR and normotensive rats. Denervation produced a significant shift to the left in the concentration-response curve to norepinephrine only in SHR vessels. Contractile responses to electrical stimulation, tyramine, and potassium were similar in both groups before denervation. Contractile responses to potassium-free solution were greater in SHR than in normotensive vessels. Following denervation, the SHR and normotensive vessels responded similarly to these latter interventions. Blockade of alpha-adrenoceptors with phentolamine reduced contractile responses to all agents in innervated and denervated vessels. Cocaine caused a slowing of the relaxation following contraction induced by electrical stimulation in both SHR and normotensive vessels. The relaxation of SHR vessels was less affected by cocaine than in normotensive vessels. The tissue content of norepinephrine was similar in SHR and normotensive arterial strips. In arterial strips from SHR the uptake of 3H-norepinephrine was significantly larger than in those from normotensive rats. The results suggest that the reactivity of innervated blood vessels to norepinephrine is similar in SHR and normotensive rats. Important differences in sensitivity to norepinephrine in hypertensive vessels are unmasked when the relationship between the vascular smooth muscle cell and the adrenergic nerve terminal is altered. Apparently, the adrenergic nerve terminals in hypertensive blood vessel can modulate the junctional concentration of norepinephrine so that the contractile response to this agent is similar to that in normotensive blood vessels.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/en_US
dc.relation.ispartofHypertensionen_US
dc.subject.meshAnimalsen_US
dc.subject.meshArteries - Analysisen_US
dc.subject.meshCocaine - Pharmacologyen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshFemaleen_US
dc.subject.meshHydroxydopamines - Pharmacologyen_US
dc.subject.meshHypertension - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshMuscle Contraction - Drug Effectsen_US
dc.subject.meshMuscle, Smooth, Vascular - Physiopathologyen_US
dc.subject.meshNeurons - Metabolismen_US
dc.subject.meshNorepinephrine - Analysis - Pharmacologyen_US
dc.subject.meshPotassium - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshReceptors, Adrenergic, Alpha - Physiologyen_US
dc.subject.meshSympathetic Nervous System - Physiopathologyen_US
dc.subject.meshSynaptic Transmissionen_US
dc.subject.meshTyramine - Pharmacologyen_US
dc.titleAdrenergic neurotransmission in vascular smooth muscle from spontaneously hypertensive ratsen_US
dc.typeArticleen_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1161/01.HYP.3.1.93-
dc.identifier.pmid6259061-
dc.identifier.scopuseid_2-s2.0-0019365572en_US
dc.identifier.volume3en_US
dc.identifier.issue1en_US
dc.identifier.spage93en_US
dc.identifier.epage103en_US
dc.identifier.isiWOS:A1981KW92500016-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWebb, RC=6603072737en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.scopusauthoridBohr, DF=7004979426en_US

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