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Decreased renal expression of nitric oxide synthase isoforms in adrenocorticotropin-induced and corticosterone-induced hypertension

Lou, Yi-kun; Wen, Cheng; Li, Ming; Adams, David; Wang, Min-xia; Yang, Feng; Morris, Brian; Whitworth, Judith

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Administration of adrenocorticotropic hormone (ACTH) leads to the development of hypertension. Because glucocorticoids can affect the nitric oxide system at several sites, the present study tested the hypothesis that nitric oxide synthase (NOS) expression may be altered in ACTH-induced and corticosterone-induced hypertension in the rat. This was addressed by measuring Nos1, Nos2, and Nos3 mRNA in the kidney, adrenal gland, heart, and hypothalamus of 16 ACTH-treated and 16 vehicle-treated rats...[Show more]

dc.contributor.authorLou, Yi-kun
dc.contributor.authorWen, Cheng
dc.contributor.authorLi, Ming
dc.contributor.authorAdams, David
dc.contributor.authorWang, Min-xia
dc.contributor.authorYang, Feng
dc.contributor.authorMorris, Brian
dc.contributor.authorWhitworth, Judith
dc.date.accessioned2015-12-13T23:20:26Z
dc.identifier.issn0194-911X
dc.identifier.urihttp://hdl.handle.net/1885/90705
dc.description.abstractAdministration of adrenocorticotropic hormone (ACTH) leads to the development of hypertension. Because glucocorticoids can affect the nitric oxide system at several sites, the present study tested the hypothesis that nitric oxide synthase (NOS) expression may be altered in ACTH-induced and corticosterone-induced hypertension in the rat. This was addressed by measuring Nos1, Nos2, and Nos3 mRNA in the kidney, adrenal gland, heart, and hypothalamus of 16 ACTH-treated and 16 vehicle-treated rats as well as in 10 corticosterone-treated and 10 control rats. In addition, in situ hybridization and immunohistochemistry were used to confirm changes by detection of Nos in RNA and NOS protein in tissues. Systolic blood pressure of ACTH and corticosterone rats was elevated (165 ± 6 and 162 ± 11 mm Hg; P<0.001 versus control). Each Nos isoform mRNA was measured by reverse transcriptase-polymerase chain reaction technique. In ACTH rats, mRNA for Nos2 was reduced in renal cortex by 58±5% and in medulla by 68±7%; for Nos3, mRNA reductions of 59±6% and 51±11% were seen (P<0.001 after Hochberg correction for multiple comparisons). In corticosterone rats, Nos2 mRNA decreased in cortex by 68±5% and in medulla by 62±6%; Nos3 mRNA by 50±8% in cortex, and Nos1 by 29±7% in medulla (all P<0.001 after Hochberg correction). Reductions seen in kidney were supported by in situ hybridization and immunohistochemistry. Apart from a 62±2% decrease in Nos2 mRNA in adrenal of ACTH rats (corrected P<0.05), no significant changes were seen in the other nonrenal tissues for any isoform. In conclusion, we have shown for the first time that the physiological components of glucocorticoid action (ACTH and corticosterone) when given chronically in vivo reduce Nos2 and Nos3 expression in the kidney. Such changes are consistent with a role in hypertension for ACTH and corticosterone.
dc.publisherLippincott Williams & Wilkins
dc.sourceHypertension
dc.subjectKeywords: corticosterone; corticotropin; isoenzyme; messenger RNA; nitric oxide synthase; RNA; tetracosactide zinc phosphate; adrenal gland; animal experiment; animal model; animal tissue; article; controlled study; heart; hypertension; hypothalamus; immunohistoche Hybridization; Immunohistochemistry; Isoenzymes; Nitric oxide; Reverse transcriptase-polymerase chain reaction; RNA
dc.titleDecreased renal expression of nitric oxide synthase isoforms in adrenocorticotropin-induced and corticosterone-induced hypertension
dc.typeJournal article
local.description.notesImported from ARIES
local.description.refereedYes
local.identifier.citationvolume37
dc.date.issued2001
local.identifier.absfor110302 - Clinical Chemistry (diagnostics)
local.identifier.ariespublicationMigratedxPub21141
local.type.statusPublished Version
local.contributor.affiliationLou, Yi-kun, University of Sydney
local.contributor.affiliationWen, Cheng, University of Sydney
local.contributor.affiliationLi, Ming, University of Sydney
local.contributor.affiliationAdams, David, University of Queensland
local.contributor.affiliationWang, Min-xia, University of Sydney
local.contributor.affiliationYang, Feng, University of Sydney
local.contributor.affiliationMorris, Brian, University of Sydney
local.contributor.affiliationWhitworth, Judith, College of Medicine, Biology and Environment, ANU
local.description.embargo2037-12-31
local.bibliographicCitation.issue4
local.bibliographicCitation.startpage1164
local.bibliographicCitation.lastpage1170
dc.date.updated2015-12-12T09:03:11Z
local.identifier.scopusID2-s2.0-0035050352
CollectionsANU Research Publications

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