on December 9, 2004
Published online before print December 9, 2004, doi: 10.1161/01.ATV.0000152610.40086.31
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Submitted on June 8, 2004
Accepted on November 22, 2004
Block of Inward Rectifying K+ Channels (KIR) Inhibits Bradykinin-Induced Vasodilatation in Human Forearm Resistance Vasculature
R. Dwivedi ;
From the Department of Clinical Pharmacology, GKT Division of Cardiovascular Medicine, St Thomas’ Hospital, London, United Kingdom.
* To whom correspondence should be addressed. E-mail: james.ritter{at}kcl.ac.uk.
Objective--To investigate the possible involvement of inward rectifying K+ channels (KIR) in the response of human resistance vessels to bradykinin in vivo.
Methods and Results--Drugs were administered via the brachial artery in healthy male volunteers and forearm blood flow was measured by venous occlusion plethysmography. Inhibition of KIR by barium chloride (4 µmol min-1) alone or with additional inhibition of Na+/K+ ATPase (ouabain 2.7 µmol min-1) reduced responses to bradykinin (30 pmol min-1), by 26±8.3% and 36±7.2%, respectively (each P<0 0.05). Barium with ouabain plus inhibitors of prostaglandin (PG) and nitric oxide synthesis inhibited but did not abolish responses to bradykinin (51±2.8% inhibition; P<0.01); norepinephrine (240 pmol min-1) caused similar reduction of baseline blood flow, as did this combination of inhibitors, but did not significantly inhibit the response to bradykinin. Barium plus ouabain did not significantly reduce responses to acetylcholine or albuterol.
Conclusion--A component of the vasodilator response to bradykinin in human forearm vasculature is mediated by KIR.
Key words: bradykinin • barium • forearm vasculature • inward-rectifying potassium channels • hyperpolarizing factor
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