Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vascular endothelial cells, which are polyfunctional, play an important role in the pathogenesis of diabetic complications. The increase in vascular permeability, ie, regulated by vascular endothelial cells, has been reported in patients with diabetes mellitus complicated by angiopathy. To determine the role of hyperglycemia in endothelial cell permeability, we examined the effect of high concentrations of glucose on the permeability of cultured bovine aortic endothelial cells. The permeations of albumin and fluorescein-labeled dextran (FD) across endothelial cell monolayers were increased when cultured with a high concentration of glucose (400 mg/dL). This increased permeation of albumin but not FD was temperature-dependent and was partially reduced by adding 100 mumol/L ponalrestat (ICI 128,436, Statil; ICI, Cheshire, UK), which is an aldose reductase inhibitor. Stimulation or inhibition of Na,K-adenosine triphosphatase (ATPase) in bovine aortic endothelial cells failed to alter their permeability. These findings suggest that high concentrations of glucose enhance transendothelial permeability of albumin in part by activating the polyol pathway, but independently of Na,K-ATPase activity.
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PMID:Increased transendothelial permeation of albumin by high glucose concentration. 754 Feb 48

The cells within the vascular wall act as a unit regulating the contraction of smooth muscle cells. In arteries the endothelium and autonomic nerves provide the major factors that regulate intracellular calcium in smooth muscle cells, which determines contractile tone. The endothelium provides a major inhibitory influence, which itself is modulated by shear forces within the vascular lumen regulating endothelial cell calcium and the release of endothelium-derived relaxing factors. Of the major mechanisms controlling smooth muscle calcium, it has been suggested that voltage-dependent calcium channels are among the most important in mediating the inhibitory influence of the endothelium. Smooth muscle potassium channels and sodium-potassium adenosine triphosphatase (Na+,K(+)-ATPase) are important regulators of membrane potential, and each is affected by the endothelium. Because the activity of each hyperpolarizes the membrane potential, they counter the influence on voltage-dependent calcium channels and inhibit contraction. Both of these counterregulatory mechanisms have recently been shown to be impaired in diseased arteries. This may help to explain the diminished effectiveness of the endothelium on the smooth muscle. Thus, vascular disease may cause diminished release, increased destruction, or limited effectiveness of endothelium-derived relaxing factors. The failure of the inhibitory influence of the endothelium may be the principal mechanism by which vascular risk factors and disease increase vasoconstrictor tone, possibly contributing to hypertension and the progression of atherosclerosis.
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PMID:Pathways controlling healthy and diseased arterial smooth muscle. 837