[State of intracellular signaling systems in endothelial dysfunction].
To estimate the state of different parts of intracellular signaling system associated with NO production after a2-adrenoreceptors stimulation under endothelial dysfunction in 22 patients with diabetic foot, the inhibitory analysis of clophelin-induced platelets aggregation modulation by administration of eNOS stimulator (L-arginin) and inhibitor (L-NAME), modulator of Ca-calmoduline (triphtazine), guanilate cyclase stimulator (sodium nitroprusside), inhibitors of phosphodiesterases (theophillinum) and protein kinase A (butamide). It was shown that endothelial dysfunction in patients with diabetic foot is associated with alteration of adrenoreactivity and inhibition of eNOS, guanilate cyclase, protein kinase A and stimulation of phosphodiesterases activity.
Barinova
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Sulaieva
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D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000328:Adult; D000368:Aged; D001120:Arginine / Q000494:pharmacology; D003000:Clonidine / Q000494:pharmacology; D017719:Diabetic Foot / Q000097:blood / Q000201:enzymology / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000201:enzymology / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D019331:NG-Nitroarginine Methyl Ester / Q000494:pharmacology; D009569:Nitric Oxide / Q000096:biosynthesis*; D052250:Nitric Oxide Synthase Type III / Q000037:antagonists & inhibitors / Q000378:metabolism; D010974:Platelet Aggregation / Q000187:drug effects*; D011941:Receptors, Adrenergic / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects
D000316:Adrenergic alpha-Agonists; D011941:Receptors, Adrenergic; D009569:Nitric Oxide; D001120:Arginine; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; D003000:Clonidine; D019331:NG-Nitroarginine Methyl Ester