| The role of aldosterone in mediating the dependence of angiotensin hypertension on IL-6. | |
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MedLine Citation:
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PMID: 19812355 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Knockout (KO) of IL-6 has been shown to attenuate ANG II hypertension, and mineralocorticoid receptors (MR) have been reported to contribute to the increase in IL-6 during acute ANG II infusion. This study determined whether that MR action is sustained with chronic ANG II infusion and whether it plays a role in mediating ANG II hypertension. ANG II infusion (90 ng/min) increased plasma IL-6 from 1.6 +/- 0.6 to 22.7 +/- 2.2 and 19.9 +/- 3.2 pg/ml on days 7 and 14, respectively, and chronic MR blockade with spironolactone attenuated that only at day 7 (7.2 +/- 2.2 pg/ml). ANG II increased MAP (19 h/day with telemetry) approximately 40 mmHg, but in ANG II+spironolactone mice (25 or 50 mg*kg(-1)*day(-1)), mean arterial pressure (MAP) was not significantly different despite a tendency for lower pressure the first 6 days. To isolate further the mineralocorticoid link to IL-6 and blood pressure, DOCA-salt hypertension was induced in IL-6 KO and wild-type (WT) mice. Plasma IL-6 increased from 4.1 +/- 1.7 to 34.5 +/- 7.0 pg/ml by day 7 of DOCA treatment in the WT mice but was back to control levels by day 14. An IL-6 bioassay using the murine B9, B-cell hybridoma cell line demonstrated that plasma IL-6 measurements reflected actual IL-6 bioactivity. The hypertension was not different and virtually superimposable in WT vs. IL-6 KO mice, averaging 145 +/- 2 and 144 +/- 3 mmHg, respectively. Both experiments confirm chronic stimulation of IL-6 by mineralocorticoids but show that it is transient. In addition, IL-6 was not required for mineralocorticoid hypertension. This suggests that aldosterone contributes to the increase in plasma IL-6 in the early stage of ANG II hypertension but that the blood pressure actions of IL-6 in that model are linked most likely to ANG II rather than aldosterone. |
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Authors:
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LaShon C Sturgis; Joseph G Cannon; Derek A Schreihofer; Michael W Brands |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-10-07 |
Journal Detail:
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Title: American journal of physiology. Regulatory, integrative and comparative physiology Volume: 297 ISSN: 1522-1490 ISO Abbreviation: Am. J. Physiol. Regul. Integr. Comp. Physiol. Publication Date: 2009 Dec |
Date Detail:
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Created Date: 2009-11-25 Completed Date: 2009-12-11 Revised Date: 2011-03-03 |
Medline Journal Info:
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Nlm Unique ID: 100901230 Medline TA: Am J Physiol Regul Integr Comp Physiol Country: United States |
Other Details:
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Languages: eng Pagination: R1742-8 Citation Subset: IM |
Affiliation:
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Department of Physiology, Medical College of Georgia, Augusta, Georgia 30912-3000, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Aldosterone
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metabolism* Aldosterone Antagonists / pharmacology Angiotensins / administration & dosage Animals Antihypertensive Agents / pharmacology Blood Pressure* / drug effects Desoxycorticosterone Disease Models, Animal Hypertension / chemically induced, drug therapy, immunology, metabolism*, physiopathology Infusion Pumps, Implantable Infusions, Subcutaneous Interleukin-6 / blood, deficiency, genetics, metabolism* Male Mice Mice, Inbred C57BL Mice, Knockout Spironolactone / pharmacology Time Factors |
| Grant Support | |
ID/Acronym/Agency:
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HL56259/HL/NHLBI NIH HHS; HL74167/HL/NHLBI NIH HHS; HL75625/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Aldosterone Antagonists; 0/Angiotensins; 0/Antihypertensive Agents; 0/Interleukin-6; 52-01-7/Spironolactone; 52-39-1/Aldosterone; 64-85-7/Desoxycorticosterone |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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