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Article: Increased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal hypertensive rats

TitleIncreased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal hypertensive rats
Authors
Issue Date1978
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.org
Citation
Circulation Research, 1978, v. 43 n. 4, p. 544-552 How to Cite?
AbstractWe isolated and perfused both the 'clipped' and 'contralateral' kidneys from Goldblatt renal hypertensive and sham-operated control rats, 1-104 days postoperatively. Responses to renal nerve stimulation were depressed in clipped kidneys from hypertensive rats (1 day postoperative), and these kidneys were supersensitive to exogenous norepinephrine (1-31 days) when compared with the contralateral organ of the same animal. Similar alterations were found between clipped and contralateral kidneys from sham-operated control rats. There was no difference in responses to renal nerve stimulation of norepinephrine between clipped kidneys from hypertensive and control rats, but clipped kidneys from hypertensive rats were supersensitive to angiotensin II (17 and 31 days). Comparison of contralateral kidneys from hypersensitive and control rats revealed no change in norepinephrine sensitivity or in responses to renal nerve stimulation, but there was a reduction in the slope of the dose-response curve to norepinephrine and of the maximal effect of the catecholamine (104 days) and a pronounced supersensitivity to angiotensin II (17-104 days) in the hypertensive rats. These results indicate that renal nerve function and norepinephrine sensitivity of the isolated renal vasculature are unchanged in renal hypertension, but clipping partially denervates the kidneys causing depressed nerve function and unilateral norepinephrine supersensitivity, unrelated to hypertension; the prolonged high pressure load on the contralateral kidney may impair the function of the vascular smooth muscle; and bilateral supersensitivity to angiotensin II is associated with hypertension but is not solely a consequence of the high pressure.
Persistent Identifierhttp://hdl.handle.net/10722/170558
ISSN
2015 Impact Factor: 11.551
2015 SCImago Journal Rankings: 5.755
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorCollis, MGen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:09:55Z-
dc.date.available2012-10-30T06:09:55Z-
dc.date.issued1978en_US
dc.identifier.citationCirculation Research, 1978, v. 43 n. 4, p. 544-552en_US
dc.identifier.issn0009-7330en_US
dc.identifier.urihttp://hdl.handle.net/10722/170558-
dc.description.abstractWe isolated and perfused both the 'clipped' and 'contralateral' kidneys from Goldblatt renal hypertensive and sham-operated control rats, 1-104 days postoperatively. Responses to renal nerve stimulation were depressed in clipped kidneys from hypertensive rats (1 day postoperative), and these kidneys were supersensitive to exogenous norepinephrine (1-31 days) when compared with the contralateral organ of the same animal. Similar alterations were found between clipped and contralateral kidneys from sham-operated control rats. There was no difference in responses to renal nerve stimulation of norepinephrine between clipped kidneys from hypertensive and control rats, but clipped kidneys from hypertensive rats were supersensitive to angiotensin II (17 and 31 days). Comparison of contralateral kidneys from hypersensitive and control rats revealed no change in norepinephrine sensitivity or in responses to renal nerve stimulation, but there was a reduction in the slope of the dose-response curve to norepinephrine and of the maximal effect of the catecholamine (104 days) and a pronounced supersensitivity to angiotensin II (17-104 days) in the hypertensive rats. These results indicate that renal nerve function and norepinephrine sensitivity of the isolated renal vasculature are unchanged in renal hypertension, but clipping partially denervates the kidneys causing depressed nerve function and unilateral norepinephrine supersensitivity, unrelated to hypertension; the prolonged high pressure load on the contralateral kidney may impair the function of the vascular smooth muscle; and bilateral supersensitivity to angiotensin II is associated with hypertension but is not solely a consequence of the high pressure.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://circres.ahajournals.orgen_US
dc.relation.ispartofCirculation Researchen_US
dc.subject.meshAngiotensin Ii - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshFemaleen_US
dc.subject.meshHypertension, Renal - Physiopathologyen_US
dc.subject.meshHypertension, Renovascular - Physiopathologyen_US
dc.subject.meshKidney - Innervationen_US
dc.subject.meshMaleen_US
dc.subject.meshNorepinephrine - Pharmacologyen_US
dc.subject.meshRatsen_US
dc.subject.meshRegional Blood Flow - Drug Effectsen_US
dc.subject.meshRenal Artery - Drug Effectsen_US
dc.titleIncreased renal vascular reactivity to angiotensin II but not to nerve stimulation or exogenous norepinephrine in renal 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.pmid688557-
dc.identifier.scopuseid_2-s2.0-0018125446en_US
dc.identifier.volume43en_US
dc.identifier.issue4en_US
dc.identifier.spage544en_US
dc.identifier.epage552en_US
dc.identifier.isiWOS:A1978FS75600009-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCollis, MG=7005797278en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US

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