Document Detail


Reactive oxygen species in essential hypertension and non-insulin-dependent diabetes mellitus.
MedLine Citation:
PMID:  10619578     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
To evaluate whether increased levels of reactive oxygen species (ROS) are involved in the pathogenesis of essential hypertension (EH) and non-insulin-dependent diabetes mellitus (NIDDM), both resting and stimulated levels of intracellular ROS were measured in lymphocytes from patients with EH (n = 10), NIDDM (n = 16) and age-matched healthy individuals (control subjects, n = 19). ROS was monitored with the dye, dihydrorhodamine-123 (DHR; 1 micromol/L) in the presence or absence of superoxide dismutase (superoxide scavenger), sodium azide (singlet oxygen/hydrogen peroxide scavenger), genistein (tyrosine kinase inhibitor), or bisindolylmaleimide (protein kinase C inhibitor). Simultaneous monitoring of cytosolic [Ca2+]i was done with fura-2. Resting ROS levels were significantly higher in NIDDM (4.71+/-0.25 nmol/10(6) cells; mean +/- SEM, P<.05) compared with EH (4.03+/-0.22 nmol/10(6) cells) or controls (4.05+/-0.15 nmol/10(6) cells). The formyl-Met-Leu-Phenylalanine-(fMLP)-induced ROS generation was significantly higher in NIDDM (21.92+/-2.23 nmol/10(6) cells; P<.05) compared with EH (14.58+/-1.90 nmol/10(6) cells) or control (16.06+/-1.22 nmol/10(6) cells). The fMLP-induced ROS increase was significantly reduced in the presence of sodium azide in all groups (P<.01) but was largely unaffected in the presence of SOD. Genistein and bisindolylmaleimide significantly inhibited the fMLP-induced ROS in all groups. The fMLP-induced [Ca2+]i increase was significantly higher in NIDDM (71+/-12 nmol/L, P <.01) compared with EH (42+/-4 nmol/L) and control subjects (35+/-3 nmol/L). Phytohemagglutinin was more effective in increasing [Ca2+]i than ROS. It is concluded that ROS may play a role in the metabolic syndrome of NIDDM but not in EH.
Authors:
N N Orie; W Zidek; M Tepel
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of hypertension     Volume:  12     ISSN:  0895-7061     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  1999 Dec 
Date Detail:
Created Date:  2000-01-20     Completed Date:  2000-01-20     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1169-74     Citation Subset:  IM    
Affiliation:
Universitätsklinik Marienhospital, University of Bochum, Germany.
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MeSH Terms
Descriptor/Qualifier:
Biological Markers / blood
Blood Pressure
Calcium / metabolism
Cytosol / metabolism
Diabetes Mellitus, Type 2 / blood*
Enzyme Inhibitors / pharmacology
Fluorescent Dyes / diagnostic use
Fura-2 / metabolism
Humans
Hypertension / blood*
Intracellular Fluid / metabolism
Lymphocyte Activation / drug effects
Lymphocytes / drug effects,  metabolism*
Middle Aged
N-Formylmethionine Leucyl-Phenylalanine / pharmacology
Oxidative Stress
Protein Kinase C / antagonists & inhibitors
Protein-Tyrosine Kinases / antagonists & inhibitors
Reactive Oxygen Species / metabolism*
Rhodamines / metabolism
Superoxide Dismutase / pharmacology
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Enzyme Inhibitors; 0/Fluorescent Dyes; 0/Reactive Oxygen Species; 0/Rhodamines; 109244-58-8/dihydrorhodamine 123; 59880-97-6/N-Formylmethionine Leucyl-Phenylalanine; 7440-70-2/Calcium; 96314-98-6/Fura-2; EC 1.15.1.1/Superoxide Dismutase; EC 2.7.10.1/Protein-Tyrosine Kinases; EC 2.7.11.13/Protein Kinase C

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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