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Article: Renal vascular reactivity in the young spontaneously hypertensive rat

TitleRenal vascular reactivity in the young spontaneously hypertensive rat
Authors
Issue Date1980
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://hyper.ahajournals.org/
Citation
Hypertension, 1980, v. 2 n. 1, p. 45-52 How to Cite?
AbstractThe renal resistance vessels of the mature spontaneously hypertensive rat (SHR) exhibit increased reactivity to vasoconstrictor agonists. This could be a cause or consequence of hypertension. We have compared vascular reactivity in isolated perfused kidneys from 46-day-old SHR and from normotensive control rats. The amplitude of responses in kidneys from the the SHR to angiotensin II, barium chloride, or norepinephrine was not different from the control. Therefore, increased reactivity of the renal vascular smooth muscle cannot be an early pathogenic mechanism in spontaneous hypertension. Responses evoked by 5-hydroxytryptamine (serotonin) were of a greater amplitude in the SHR than in the control kidney. However, this difference was due to interaction of serotonin with the sympathetic nerves, as it was abolished by treatment of the rats with 6-hydroxydopamine. Responses induced by electrical stimulation of the renal sympathetic nerves were also of greater amplitude in SHR than in control kidneys, both before and after the blockade of norepinephrine disposition mechanisms. Nerve stimulation evoked a greater efflux of endogenous norepinephrine from kidneys of the SHR than from those of control rats. Thus, the increased reactivity of the SHR kidney to renal nerve stimulation is due to an augmented release of endogenous norepinephrine. This could be an important factor in the early development of hypertension.
Persistent Identifierhttp://hdl.handle.net/10722/170615
ISSN
2015 Impact Factor: 6.294
2015 SCImago Journal Rankings: 3.702
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCollis, MGen_US
dc.contributor.authorDemey, Cen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:10:09Z-
dc.date.available2012-10-30T06:10:09Z-
dc.date.issued1980en_US
dc.identifier.citationHypertension, 1980, v. 2 n. 1, p. 45-52en_US
dc.identifier.issn0194-911Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/170615-
dc.description.abstractThe renal resistance vessels of the mature spontaneously hypertensive rat (SHR) exhibit increased reactivity to vasoconstrictor agonists. This could be a cause or consequence of hypertension. We have compared vascular reactivity in isolated perfused kidneys from 46-day-old SHR and from normotensive control rats. The amplitude of responses in kidneys from the the SHR to angiotensin II, barium chloride, or norepinephrine was not different from the control. Therefore, increased reactivity of the renal vascular smooth muscle cannot be an early pathogenic mechanism in spontaneous hypertension. Responses evoked by 5-hydroxytryptamine (serotonin) were of a greater amplitude in the SHR than in the control kidney. However, this difference was due to interaction of serotonin with the sympathetic nerves, as it was abolished by treatment of the rats with 6-hydroxydopamine. Responses induced by electrical stimulation of the renal sympathetic nerves were also of greater amplitude in SHR than in control kidneys, both before and after the blockade of norepinephrine disposition mechanisms. Nerve stimulation evoked a greater efflux of endogenous norepinephrine from kidneys of the SHR than from those of control rats. Thus, the increased reactivity of the SHR kidney to renal nerve stimulation is due to an augmented release of endogenous norepinephrine. This could be an important factor in the early development of hypertension.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.mesh5-Hydroxytryptophan - Pharmacologyen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBarium - Pharmacologyen_US
dc.subject.meshBlood Pressure - Drug Effectsen_US
dc.subject.meshChemotherapy, Cancer, Regional Perfusionen_US
dc.subject.meshElectric Stimulationen_US
dc.subject.meshHypertension, Renal - Physiopathologyen_US
dc.subject.meshHypertension, Renovascular - Physiopathologyen_US
dc.subject.meshKidney - Blood Supply - Innervation - Physiopathologyen_US
dc.subject.meshMaleen_US
dc.subject.meshNorepinephrine - Blood - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshSympathetic Nervous System - Physiologyen_US
dc.subject.meshVasoconstriction - Drug Effectsen_US
dc.titleRenal vascular reactivity in the young spontaneously hypertensive raten_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.2.1.45-
dc.identifier.pmid6966255-
dc.identifier.scopuseid_2-s2.0-0019190925en_US
dc.identifier.volume2en_US
dc.identifier.issue1en_US
dc.identifier.spage45en_US
dc.identifier.epage52en_US
dc.identifier.isiWOS:A1980JB88200007-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCollis, MG=7005797278en_US
dc.identifier.scopusauthoridDeMey, C=6506528726en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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