Document Detail


Angiotensin II regulates adrenal vascular tone through zona glomerulosa cell-derived EETs and DHETs.
MedLine Citation:
PMID:  21199991     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Elevated concentrations of aldosterone are associated with several cardiovascular diseases. Angiotensin II (Ang II) increases aldosterone secretion and adrenal blood flow. This concurrent increase in steroidogenesis and adrenal blood flow is not understood. We investigated the role of zona glomerulosa (ZG) cells in the regulation of vascular tone of bovine adrenal cortical arteries by Ang II. ZG cells enhanced endothelium-dependent relaxations to Ang II. The ZG cell-dependent relaxations to Ang II were unchanged by removing the endothelium-dependent response to Ang II. These ZG cell-mediated relaxations were ablated by cytochrome P450 inhibition, epoxyeicosatrienoic acid (EET) antagonism, and potassium channel blockade. Analysis of ZG cell EET production by liquid chromatography/mass spectrometry demonstrated an increase in EETs and dihydroxyeicosatrienoic acids with Ang II stimulation. These EETs and dihydroxyeicosatrienoic acids produced similar concentration-dependent relaxations of adrenal arteries, which were attenuated by EET antagonism. Whole-cell potassium currents of adrenal artery smooth muscle cells were increased by Ang II stimulation in the presence of ZG cells but decreased in the absence of ZG cells. This increase in potassium current was abolished by iberiotoxin. Similarly, 14,15-EET induced concentration-dependent increases in potassium current, which was abolished by iberiotoxin. ZG cell aldosterone release was not directly altered by EETs. These data suggest that Ang II stimulates ZG cells to release EETs and dihydroxyeicosatrienoic acids, resulting in potassium channel activation and relaxation of adrenal arteries. This provides a mechanism by which Ang II concurrently increases adrenal blood flow and steroidogenesis.
Authors:
Phillip G Kopf; Kathryn M Gauthier; David X Zhang; John R Falck; William B Campbell
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-01-03
Journal Detail:
Title:  Hypertension     Volume:  57     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-01-20     Completed Date:  2011-04-22     Revised Date:  2013-09-19    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  323-9     Citation Subset:  IM    
Affiliation:
Department of Pharmacology and Toxicology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
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MeSH Terms
Descriptor/Qualifier:
8,11,14-Eicosatrienoic Acid / analogs & derivatives*,  metabolism,  pharmacology
Adrenal Glands / blood supply
Aldosterone / metabolism
Angiotensin II / pharmacology*
Animals
Arachidonic Acid / metabolism
Arteries / drug effects*,  physiology
Cattle
Cells, Cultured
Dose-Response Relationship, Drug
Epoxide Hydrolases / metabolism
Membrane Potentials / drug effects
Muscle, Smooth, Vascular / cytology,  drug effects,  physiology
Myocytes, Smooth Muscle / drug effects,  physiology
Patch-Clamp Techniques
Potassium Channels / physiology
Vasoconstrictor Agents / pharmacology
Vasodilation / drug effects
Vasodilator Agents / metabolism,  pharmacology
Zona Glomerulosa / cytology,  drug effects,  metabolism
Grant Support
ID/Acronym/Agency:
GM31278/GM/NIGMS NIH HHS; HL-83297/HL/NHLBI NIH HHS; P01 DK038226/DK/NIDDK NIH HHS; R01 GM031278-27/GM/NIGMS NIH HHS; R01 HL083297/HL/NHLBI NIH HHS; R01 HL083297-05/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/14,15-dihydroxyeicosatrienoic acid; 0/Potassium Channels; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 11128-99-7/Angiotensin II; 506-32-1/Arachidonic Acid; 52-39-1/Aldosterone; 7324-41-6/8,11,14-Eicosatrienoic Acid; 81276-03-1/14,15-epoxy-5,8,11-eicosatrienoic acid; EC 3.3.2.-/Epoxide Hydrolases
Comments/Corrections

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