Mechanisms of decreased bradykinin-induced vasodilation in experimental hyperlipemia-hyperglycemia: Contribution of nitric oxide and CA2+-activated K+ channels

Fundamental and Clinical Pharmacology

Volumn 15, Issue 5, 2001, Pages 335-342

  Georgescu, A ^a   Popov, D ^a   Simionescu, M ^a  

^a INSTITUTE OF CELLULAR BIOLOGY AND PATHOLOGY NICOLAE SIMIONESCU   (Romania)

Author keywords

Bradykinin; Diabetes; L arginine; NO dependent relaxation; NO independent relaxation; Resistance arteries

Indexed keywords

ARGININE; ARGININE METHYL ESTER; BRADYKININ; CALCIUM CHANNEL; CALCIUM ION; LIPID; NITRIC OXIDE SYNTHASE; NITROPRUSSIDE SODIUM; POTASSIUM CHANNEL; POTASSIUM ION; STREPTOZOCIN; TETRYLAMMONIUM;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTERY RESISTANCE; ARTICLE; ATHEROSCLEROSIS; BLOOD VESSEL REACTIVITY; COMPARATIVE STUDY; CONTROLLED STUDY; DIABETES MELLITUS; DRUG MECHANISM; HAMSTER; HYPERGLYCEMIA; HYPERLIPIDEMIA; LIPID DIET; MALE; MYOGRAPHY; NONHUMAN; PRIORITY JOURNAL; VASCULAR DISEASE; VASODILATATION;

ANIMALS; BRADYKININ; CRICETINAE; DIABETES MELLITUS, EXPERIMENTAL; ENDOTHELIUM, VASCULAR; HYPERLIPIDEMIAS; MALE; MESENTERIC ARTERIES; MESOCRICETUS; NITRIC OXIDE; NITRIC OXIDE SYNTHASE; POTASSIUM CHANNELS, CALCIUM-ACTIVATED; VASCULAR RESISTANCE; VASODILATION;

EID: 0035679170     PISSN: 07673981     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1472-8206.2001.00047.x     Document Type: Article

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