Ischaemia enhances the role of Ca2+-activated K+ channels in endothelium-dependent and nitric oxide-mediated dilatation of the rat hindquarters vasculature

Clinical and Experimental Pharmacology and Physiology

Volumn 31, Issue 4, 2004, Pages 254-260

  Woodman, Owen L ^a   Wongsawatkul, Orapin ^a  

^a UNIVERSITY OF MELBOURNE   (Australia)

Author keywords

BKCa channels; Dilatation; Endothelium; Ischaemia; Nitric oxide

Indexed keywords

CALCIUM ACTIVATED POTASSIUM CHANNEL; CALCIUM ION; GLIBENCLAMIDE; N(G) NITROARGININE; NITRIC OXIDE; NITRIC OXIDE SYNTHASE INHIBITOR; NITROPRUSSIDE SODIUM; POTASSIUM CHANNEL; SODIUM CHLORIDE; TETRYLAMMONIUM;

ANIMAL MODEL; ARTICLE; ATTENUATION; CONTROLLED STUDY; DRUG DOSE REDUCTION; DRUG EFFECT; DRUG INHIBITION; FEMALE; ISCHEMIA; NONHUMAN; PHYSIOLOGY; RAT; REDUCTION; REPERFUSION; VASCULARIZATION; VASODILATATION;

ANIMALS; CALCIUM CHANNEL BLOCKERS; DOSE-RESPONSE RELATIONSHIP, DRUG; ENDOTHELIUM, VASCULAR; FEMALE; HINDLIMB; ISCHEMIA; NITRIC OXIDE; NITROARGININE; POTASSIUM CHANNELS; POTASSIUM CHANNELS, CALCIUM-ACTIVATED; RATS; RATS, SPRAGUE-DAWLEY; VASODILATION;

EID: 1942473762     PISSN: 03051870     EISSN: None     Source Type: Journal    
DOI: 10.1111/j.1440-1681.2004.03987.x     Document Type: Article

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