Abstract
The endothelium plays a crucial role in the regulation of the vessel wall under physiological and pathological conditions.1 The endothelium lines all vessels of the body and is the most important structure for communication between the blood stream and the vessel wall.2 One function is to act as a barrier that prevents noxious agents from entering the vessel wall. Other functions of healthy endothelium include antithrombotic properties that inhibit the adhesion of blood cells (thrombocytes, erythrocytes, and leukocytes) to the vessel wall. Hence, endothelial cells are crucial for maintaining laminar blood flow. A third function of the endothelium is a secretory function. Endothelial cells can release their secretory products into the vessel wall as well as into the blood stream. Of particular importance for the physiological function of the vessel wall is the vasorelaxing function of endothelial cells1 due to secretion of endothelium-derived relaxing factor (EDRF).3 Under physiological conditions, EDRF is released permanently and ensures the patency of normal vessels.4 In addition, endothelial cells can release vasoconstrictive factors such as endothelin into the vessel wall.5,6 Furthermore, studies over recent years have identified growth factors and chemotactic substances which are produced by damaged or overstimulated endothelial cells and which play a crucial part in structural changes of the vessel wall.7,8
This is a preview of subscription content, log in via an institution.
Buying options
Tax calculation will be finalised at checkout
Purchases are for personal use only
Learn about institutional subscriptionsPreview
Unable to display preview. Download preview PDF.
References
Luscher TF, Vanhoutte PM.The endothelium: modulator of cardiovascular function. CRC Press, Boca Raton 1990
Dzau VJ, Gibbons GH. Cell biology of vascular hypertrophy in systemic hypertension. Am J Cardiol 1988;62:30G–35G.
Vallance P, Collier J, Moncada S. Effects of endothelium-derived nitric oxide on peripheral arteriolar tone in man. Lancet 1989;1:997–1000.
Luscher TF. Imbalance of endothelium-derived relaxing and- contracting factors: a new concept in hypertension? Am J Hypertens 1990;3:317–30.
Yanagisawa X, Kurihara H, Kimur S, Mitsiu Y, Kobayashi M, Watnabe TX, Masaki T.A novel potent vasoconstrictor peptide produced by vascular endothelial cells. Nature 1988;388:411–415.
Panza JA, Quyyumi AA, Brush JE Jr, Epstein SE. Endothelium-dependent vascular relaxation in patients with essential hypertension. N Engl J Med 1990;323:22–7.
DiCorleto PE, Fox PL. Growth factor production by endothelial cells. In: Una R (ed) Endothelial cells, vol 2. CRC Press, Boca Raton 1988:51–62.
Egleme C, Creesier F, Wood JM. Local formation of angiotensin II in the rat aorta. Effect of endothelium. Br J Pharmacol 1990;100:237–40.
Palmer RJM, Ashtor DS, Moncada S. Vascular endothelial cells synthesize nitroxide from L-arginine. Nature 1988;333:664–666.
Lorenzi M, Cagliero E. Pathobiology of endothelial and other vascular cells in diabetes mellitus; call for data. Diabetes 1991;40:653–659.
Jensen T, Bjerre-Knudsen J, Feldt-Rasmussen B, Deckert. Features of endothelial dysfunction in early diabetic nephropathy. Lancet 1989; 1:461–463.
Guerra R, Brotherton AFA, Goodwin PJ, Clark CR, Armstrong ML, Harrison DG. Mechanisms of abnormal endothelium-dependent vascular relaxation in atherosclerosis: implications for altered autocrine and paracrine functions of DRF. Blood Vessels 1989;26:300–314.
Ciriaco E, Abbate F, Ferrante F, Laura R, Amenta F. Structural changes in the endothelium of the femoral artery of spontaneously hypertensive rats: sensitivity to isradipine treatment. J Hypertens 1993;11:515–522.
Himmel HM, Whorton AR, Strauss HC. Intracellular calcium, currents, and stimulus - response coupling in endothelial cells. Hypertension 1993;21:112–127.
Gunther J, Dhein S, Rosen R, Klaus W, Fricke U. Nitric oxide (EDRF) enhances the vasorelaxing effect of nitrendipine in various isolated arteries. Basic Res Cardiol 1992;87:452–460.
Wilkie ME, Stevens CR, Cunningham J, Blake D. Hypoxia-induced von Willebrand factor release is blocked by verapamil. Miner Electrolyte Metab 1992; 18:141–144.
Luscher TF, Espinosa E, Dubey RK, Yang Z. Vascular biology of human coronary artery and bypass graft disease. Curr Opin Cardiol 1993;8:963–974.
Yang Z, Bauer E, von Segesser L, Stulz P, Turina M, Luscher TF. Different mobilization of calcium in endothelin-i-induced contractions in human arteries and veins: effects of calcium antagonists. J Cardiovasc Pharmacol 1990;16:654–660.
Goto K, Kasuya Y Matsuki N, Takuwa Y, Kurihara H, Kimura S, Yanagisawa M, Masaki T. Endothelin activates the dihydropyridine - sensitive, voltage-dependent calcium channel in vascular smooth muscle. Proc Natl Acad Sci USA 1989;86:3915–3918.
Kiowski W, Luscher TF, Linder L, Buhler FR. Endothelin-1 induced vasoconstriction in Man: reveral by calcium channel blockade but not by nitrovasodilators or EDRF. Circulation 1991;83:469–475.
Haller H, Schaberg T, Lindschau C, Quass P, Lode H, Distler A. Endothelin increases intracellular free calcium, protein phosphorylation and O2-production in human alveolar macrophages. Am J Physiol 1991;261:L713–L723.
Wright B, Zeitman I, Greig R, Poste G. Inhibition of macrophage function by calcium channel blockers and calmodulin antagonists. Cell Immunol 1985;95:46–53.
Jouvin-Marche E, Cerrina J, Coeffier E, Duroux P, Benviste J. Effect of the calcium antagonist nifedipine on the relase of PAF, slow-reacting substance and beta- glucuronidase from human neutrophils. Eur J Pharmacol 1983;89:19–26.
Haller H, Lenz T, Ludersdorf M, Distler A, Philipp T. Changes in sensitivity to angiotensin II in platelets. J Cardiovasc Pharmacol 1987;10 [Suppl 10]:S44–S46.
Tschüpe D, Kaufmann L, Roesen P, Ohlrogge R, Gries FA. Influence of a single dose of nitrendipine on whole platelet activity in healthy subjects. J Cardiovasc Pharmacol 1988;12:S167–S169.
Collins P, Rosano GM, Jiang C, Lindsay D, Sarrel PM, Poole-Wilson PA. Cardiovascular protection by oestrogen - a calcium antagonist effect? Lancet 1993;341:1264–1265.
Fleckenstein-Grun G,Frey M,Thimm F, Hofgartner W, Fleckenstein A.Calcium overload an important cellular mechanism in hypertension and arteriosclerosis.Drugs.1992;1:23–30.
Loaldi A, Polese A, Montorsi P. Comparison of nifedipine, propranolol and isosorbide dinitrate on angiographic progression and regression of coronary arterial narrowings in angina pectoris.Am J Cardiol.1989;64:433–439
Lichtlen PR, Hugenholtz PG, Rafflenbeul W, Hecker H, Jost S, Deckers JW. On behalf on the INTACT group investigators. Retardation of angiographic progression of coronary artery disease by nifedipine. Lancet 1990;335:1109–13.
Waters D, Lesperance J, Francetich M et al. A controlled clinical trial to assess the effect of calcium channel blocker on the progression of coronary atherosclerosis. Circulation 1990;82:1940–53.
Schroeder JS, Gao SZ, Alderman EL, Hunt SA, Johnstone I, Boothroyd DB, Wiederhold V, Stinson EB. A preliminary study of diltiazem in the prevention of coronary artery disease in heart transplant recipients. N Engl J Med 1993;328:164–70.
on behalf of the REGRESS study group. Effects of lipid lowering by pravastatin on progression and regression of qoronary artery disease in symptomatic men with normal to moderately elevated serum cholesterol levels. Circulation 1995;91:2528–40.
Evidence for a synergistic effect of calcium channel blockers with lipid-lowering therapy in retarding progression of coronary atherosclerosis in symptomatic patients with normal to moderately raised cholesterol levels. Arterioscier Thromb Vase Biol 1996;16:425–30.
Buchwald H, Matts JP, Fitch LL et al. for the Program on the Surgical Control of the Hyperlipidemias (POSCH) Group. Changes in sequential coronary arteriograms and subsequent coronary events. JAMA 1992;268:1429–33.
Waters D, Craven TE, Lesperance J. Prognostic significance of progression of coronary atherosclerosis. Circulation 1993;87:1067–75.
Progression of coronary artery disease predicts clinical coronary events. Long-term follow-up from the Cholesterol Lowering Atherosclerosis Study. Circulation 1996;93:34–41.
Calcium channel blockers and coronary atherosclerosis: From the rabbit to the real world. Am Heart J 1994; 1128:1309–16.
Etingin OR, Hajjar DP. Calcium channel blockers enhance cholesteryl ester hydrolysis and decrease total accumulation in human aortic tissue. Circulation Research 1990;66:185–90.
Witztum JL. The oxidation hypothesis of atherosclerosis. Lancet 1994;344:793–5.
Mak IT, Weglicki WB. Comparative antioxidant activities of propranolol, nifedipine, verapamil, and diltiazem against sarcolemmal membrane lipid peroxidation. Circ Res 1990;66:1449–52.
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1997 Kluwer Academic Publishers
About this chapter
Cite this chapter
Vliegen, H.W., Jukema, J.W., van der Laarse, A., Haller, H. (1997). Endothelial Function and Calcium Metabolism. In: van der Wall, E.E., Cats, V.M., Baan, J. (eds) Vascular Medicine. Developments in Cardiovascular Medicine, vol 197. Springer, Dordrecht. https://doi.org/10.1007/978-94-009-0037-0_5
Download citation
DOI: https://doi.org/10.1007/978-94-009-0037-0_5
Publisher Name: Springer, Dordrecht
Print ISBN: 978-94-010-6505-4
Online ISBN: 978-94-009-0037-0
eBook Packages: Springer Book Archive