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Muscle arterial smooth

Calcium channel blockers reduce arterial blood pressure by decreasing calcium influx, resulting in a decrease in intracellular calcium (236,237). The arterial smooth muscle tone decreases, thereby decreasing total peripheral resistance. The increase in vascular resistance in hypertension is found to depend much on calcium influx. Calcium channel blockers reduce blood pressure at rest and during exercise. They decrease the transmembranous calcium influx or entry that lead to a net decrease of intracellular calcium and therefore the vascular tone falls, as does blood pressure. [Pg.141]

Furchgott RF, Zawadzki JV (1980) Obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature (Lond) 288 373-376... [Pg.860]

Dimopoulos GJ, Semba S, Kitazawa K et al (2007) Ca2+-dependent rapid Ca2+ sensitization of contraction in arterial smooth muscle. Circ Res 100 121-129... [Pg.1145]

J mohara M, Takasaki J, Matsumoto M> Matsumoto S-I, Saito X Soga X Matsushime H, Furuichi K Functional characterization of cysteinyl leukotriene CysLT2 receptor on human coronary artery smooth muscle cells. Biochem Biophys Res Commun 2001 287 1088. [Pg.109]

The intima of the arterial wall contains hyaluronic acid and chondroitin sulfate, dermatan sulfate, and heparan sulfate proteoglycans. Of these proteoglycans, dermatan sulfate binds plasma low-density lipoproteins. In addition, dermatan sulfate appears to be the major GAG synthesized by arterial smooth muscle cells. Because it is these cells that profiferate in atherosclerotic lesions in arteries, dermatan sulfate may play an important role in development of the atherosclerotic plaque. [Pg.548]

Evidence from cellular studies in vitro initially showed how oxidative processes could play a central role in the pathological changes involved in the genesis of atherosclerosis. LDL can be oxidatively modified in culture by a range of cell types including endothelial cells (Henriksen et a.1., 1981), arterial smooth muscle cells... [Pg.44]

Heinecke, J.W., Rosen, H. and Chait, A. (1984). Iron and copper promote modification of low density lipoprotein by human arterial smooth muscle cells in culture. J. Clin. Invest. 74, 1890-1894. [Pg.50]

Holland et al. [125] have shown that the potent vascular smooth muscle cell mitogen and phospholipase A2 activator thrombin stimulated superoxide production in human endothelial cells, which was inhibited by the NADPH oxidase inhibitors. Similarly, thrombin enhanced the production of oxygen species and the expression of )Alphos and Rac2 subunits of NADPH oxidase in VSMCs [126,127]. Greene et al. [128] demonstrated that the activator of NO synthase neuropeptide bradykinin is also able to stimulate NADPH oxidase in VSMCs. Similar to XO, NADPH oxidase enhanced superoxide production in pulmonary artery smooth muscle cells upon exposure to hypoxia [129]. [Pg.727]

Oxidized LDL are considered to be one of the major factors associated with the development of atherosclerosis. The earliest event is the transport of LDL into the arterial wall where LDL, being trapped in subendothelial space, are oxidized by oxygen radicals produced by endothelial and arterial smooth muscle cells. The oxidation of LDL in the arterial wall is affected by various factors including hemodynamic forces such as shear stress and stretch force. Thus, it has been shown [177] that stress force imposed on vascular smooth muscle cells incubated with native LDL increased the MDA formation by about 150% concomitantly with the enhancement of superoxide production. It was suggested that oxidation was initiated by NADPH oxidase-produced superoxide and depended on the presence of metal ions. [Pg.798]

Nitrates (e.g., ISDN) and hydralazine were combined originally in the treatment of HF because of their complementary hemodynamic actions. Nitrates are primarily venodilators, producing reductions in preload. Hydralazine is a direct vasodilator that acts predominantly on arterial smooth muscle to reduce systemic vascular resistance (SVR) and increase stroke volume and cardiac output. Evidence also suggests that the combination may provide additional benefits by interfering with the biochemical processes associated with HF progression. [Pg.103]

Bhalla RC, Toth KF, Bhatty RA, Thompson LP, Sharma RV (1997) Estrogen reduces proliferation and agonist-induced calcium increase in coronary artery smooth muscle cells. Am J Physiol 272 H 1996-2003... [Pg.238]

Lavigne MC, Ramwell PW, Clarke R (1999) Inhibition of estrogen receptor function promotes porcine coronary artery smooth muscle cell proliferation. Steroids 64 472-480... [Pg.242]

Perez GJ, Bonev AD, Nelson MT 2001 Micromolar Ca2+ from sparks activates Ca2+-sensitive K+ channels in rat cerebral artery smooth muscle. Am J Physiol Cell Physiol 281 C1769-C1775 Rembold CM 1992 Regulation of contraction and relaxation in arterial smooth muscle. Hypertension 20 129-137... [Pg.4]

Dreja K, Nordstrom I, Hellstrand P 2001 Rat arterial smooth muscle devoid of ryanodine receptor function effects on cellular Ca2+ handling. Br J Pharmacol 132 1957-1966 Martin C, Hyvelin JM, Chapman KE, Marthan R, Ashley RH, Savineau JP 1999 Pregnant rat myometrial cells show heterogeneous ryanodine- and caffeine-sensitive calcium stores. Am J Physiol 277 C243-C252... [Pg.25]

Asada Y, Yamazawa T, Hirose K, Takasaka T, lino M 1999 Dynamic Ca2+ signalling in rat arterial smooth muscle cells under the control of local renin-angiotensin system. J Physiol 521 497-505... [Pg.39]

Li PL, Tang WX, Valdivia HH, Zou AP, Campbell WB 2001 cADP-ribose activates reconstitutes ryanodine receptors from coronary arterial smooth muscle. Am J Physiol... [Pg.40]

Nelson MT, Patlak JB, Worley JF, Standen NB 1990 Calcium channels, potassium channels, and voltage dependence of arterial smooth muscle tone. Am J Physiol 259 C3-C18 Nixon GF, Mignery GA, Somlyo AV 1994 Immunogold localization of inositol 1,4,5-trisphosphate receptors and characterization of ultrastructural features of the sarcoplasmic reticulum in phasic and tonic smooth muscle. J Muscle Res Cell Motil 15 682-700 Peng H, Matchkov V, Ivarsen A, Aalkjaer C, Nilsson H 2001 Hypothesis for the initiation of vasomotion. CircRes 88 810-815... [Pg.40]

Nelson MT, Cheng H, Rubart M et al 1995 Relaxation of arterial smooth muscle by calcium sparks. Science 270 633—637... [Pg.64]

James PF, Grupp IL, Grupp G et al 1999 Identification of a specific role for the Na,K-ATPase a2 isoform as a regulator of calcium in the heart. Mol Cell 3 555—563 Janiak R, Wilson, SM, Montague S, Hume JR 2001 Heterogeneity of calcium stores and elementary release events in canine pulmonary arterial smooth muscle cells. Am J Physiol 280 C22-C33... [Pg.136]

Nelson MT, Quayle JM 1995 Physiological roles and properties of potassium channels in arterial smooth muscle. Am J Physiol 268 C799—C822... [Pg.216]

Kowarski D, Shuman H, Somlyo AP, Somlyo AV 1985 Calcium release by norepinephrine from central sarcoplasmic reticulum in rabbit main pulmonary artery smooth muscle. J Physiol 366 153-175... [Pg.267]


See other pages where Muscle arterial smooth is mentioned: [Pg.296]    [Pg.297]    [Pg.297]    [Pg.815]    [Pg.815]    [Pg.213]    [Pg.47]    [Pg.759]    [Pg.766]    [Pg.794]    [Pg.2]    [Pg.40]    [Pg.70]    [Pg.135]    [Pg.136]    [Pg.164]    [Pg.167]    [Pg.191]    [Pg.197]    [Pg.202]    [Pg.202]    [Pg.213]   
See also in sourсe #XX -- [ Pg.2 ]

See also in sourсe #XX -- [ Pg.184 , Pg.186 ]

See also in sourсe #XX -- [ Pg.11 , Pg.746 ]

See also in sourсe #XX -- [ Pg.105 ]




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