Arteries endothelium

Reichlin, T., Wild, A., Durrenberger, M., Daniels, A. U., Aebi, U., Hunziker, P. R., and Stolz, M. (2005). Investigating native coronary artery endothelium in situ and in cell culture by scanning force microscopy./. Struct. Biol. 152, 52-63. 

E. Vasile, M. Simionescu and N. Simionescu, Visualization of the binding, endocytosis and transcytosis of low-density lipoprotein in the arterial endothelium in situ, J. Cell Biol. 96 (1983) 1677-1689. 

Initial concern of possible deleterious effects of ICB on adjacent normal coronary-artery endothelium was refuted with studies showing three- and five-year follow-up results of patients randomized to PCI with IRB or PCI with placebo... 

Kaiser DR, Billups K, Mason C, et al, Impaired brachial artery endothelium-dependent and -independent vasodilation in men with erectile dysfunction and no other clinical cardiovascular disease, J Am Coll Cardiol 2004 43 (2) 179-1 84,... 

Olson, S., Oeckler, R., Li, X., et al. 2004. Angiotensin II stimulates nitric oxide production in pulmonary artery endothelium via the type 2 receptor. Am J Physiol 287 L559-L568. 

Schmidt, T., Zaib, F., Samson, S.E., Kwan, C.Y., and Grover, A.K. 2004. Peroxynitrite resistance of sarco/endoplasmic reticulum Ca2+ pump in pig coronary artery endothelium and smooth muscle. Cell Calcium 36 77-82. 

Burnham, M. P., Bychkov, R., Feletou, M., Richards, G. R., Vanhoutte, P. M., Weston, A. H., and Edwards, G. 2002. Characterization of an apamin-sensitive small-conductance Ca2+-activated K+ channel in porcine coronary artery endothelium relevance to EDHF. Br. J. Pharmacol. 135 1133-1143. 

Angiotensin I converting enzyme is a dipeptidyl carboxypeptidase that cleaves angiotensin I to angiotensin II and the dipeptide histidyl-leucine (His-Leu). The enzyme is bound to the membrane of lung arterial endothelium and is involved in the renin-angiotensin system that regulates blood pressure and fluid balance. 

Lowell Langille B (1993) Remodeling of developing and mature arteries endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol 21 (Suppl 1) S11-S17... 

Certain amount of blood platelet is the basic material for artery smc hyperplasia and fibric plaque formation. Blood platelet is attached to artery endothelium,which plays an... 

Serotonin S-hydroxytryptamine, M, 176.2, a plant and animal hormone. It is produced by hydroxylation of L-tryptophan to 5-hydroxytryptophan, followed by decarboxylation. The synthesis occurs in the central nervous system, lung, spleen and argentaffine light cells of the intestinal mucosa. S. is stored in thrombocytes and mast cells of the blood. It acts as a Neuro-transmitter (see), stimulates peristalsis of the intestine, and causes a dose-dependent constriction of smooth muscle. It stimulates the release from arterial endothelium of a dilator substance which counteracts its primary constricting effect [T.M. Cocks X A. Angus Nature 305 (1983) 627-630]. S. is a precursor of the hormone Melatonin (see). It is inactivated and degraded by monoamine oxidases and aldehyde oxidases to 5-hydroxy-indoleacetic acid. 

I believe that the clinical practice of medicine and cardiology of the future will be influenced more, much more, profoundly by studies of human genetics, molecular biology, cellular physiology and experimental pathology, by studies of problems such as the mechanisms of endocytosis as the mechanisms of on-docystosis, the control of calcium fluxes across the sarcolemma of the colemma of the myocardium and specialised cardiac tissue, the fundamental mechanisms by which platelets adhere to the arterial endothelium or by which adrenalin acts on its receptors and vascular smooth muscle the renal cortex and other tissues by all these, and other fundamental studies. It is becoming even clearer that in most... 

Leukocyte count is associated with aortic arch plaque thickness, and is specifically correlated with aortic arch plaque thickness equal to or more than 4 mm in stroke-free subjects (157). In WHHL rabbits, leukocyte adherence to intact arterial endothelium is one of the geneses and promoters of atherosclerosis (158). 

With the advent of cryopreservation techniques, it is now possible to preserve the arterial endothelium and smooth muscle cells and their properties of contractility and vessel wall relaxation (42,43). A large retrospective multicenter study examined a population in which either fresh or cryopreserved arterial allograft was used for limb salvage infrainguinal reconstruction. The data from this report demonstrated suboptimal 5-year primary and secondary patency rates of 16% and 26%, but a respectable 74% 5-year rate of limb salvage (44). While it does have drawbacks, the use of arterial allograft, either fresh or cryopreserved, represents another available conduit with which to allow reconstruction for limb salvage. 

The production of inflammatory cytokines and cell adhesion molecules (CAMs) by the arterial endothelium are key cellular events involved in the development of atherosclerosis. Activation of the endothelium results in the release of vascular cytokines such as interleukin-1 (IL-la) and tumor necrosis factor alpha (TNF-a). These cytokines induce the expression of CAMs such as intracellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1), which, together with activated monocyte chemoattractant protein-1 (MCP-1), recruit monocytes through the vascular wall, where they are involved in foam cell formation. The nuclear transcription factor, NF-kB, is a mediator in TNF-a-induced expression of cell adhesion molecules and MCP. NF-kB is activated by an atherogenic diet (Liao et al. 1993) and oxidized LDL (Brand et al. 1997), and activation is inhibited by various antioxidants (Kunsch and Medford 1999). Therefore it is of particular interest that GEN attenuated NF-kB DNA binding and TNF-a release in human monocytes (Shames et al. 1999). A small, uncontrolled pilot study ( = 6) found that GEN, but not DAI, inhibited TNF-a-induced NF-kB activation in ex vivo human lymphocytes following consumption of 100 mg isoflavones/day for 3 weeks, as well as in cultured human... 

Mohazzab KM, Kaminski PM, Wolin MS. NADH oxidoreductase is a major source of superoxide anion in bovine coronary artery endothelium. Am J Physiol 1994 266 H2568-H2572. 

There are several theories of atherogenesis and these may eventually be shown to be interactive. The lipid hypothesis suggests that persistent hyperlipidemia leads to cholesterol accumulation in the arterial endothelium. Hypercholesterolemia may activate protein growth factors, which stimulate smooth muscle cell proliferation. 

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