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Angiotensin II stimulation

Adrenal Inhibition of angiotensin II stimulated aldosterone release... [Pg.1149]

Hyperkalemia results from reduced angiotensin II-stimulated aldosterone release. The risk of hyperkalemia with ACE... [Pg.46]

JD Johnson, JC Garrison. (1987). Epidermal growth factor and angiotensin II stimulates formation of inositol 1,4,5 and inositol 1,3,4-trisphosphate in hepatocytes. J Biol Chem 262 17285-17293. [Pg.389]

C. Thorup, M. Komfeld, J.M. Winaver, M.S. Goligorsky, and L.C. Moore, Angiotensin-II stimulates nitric oxide release in isolated perfused renal resistance arteries. Pflugers Arch. 435, 432-434 (1998). [Pg.50]

Figure 22.16 Regulation of vasoconstriction/vasodilation by angiotensin-II and bradykinin. The mechanism by which angiotensin-II stimulates vasoconstriction is shown in Figure 22.15. Angiotensin-converting enzyme is also responsible for bradykinin inactivation. Bradykinin stimulates endothelial cells to produce and secrete nitric oxide and prostacyclin, both of which are vasodilators. Consequently the effect of an ACE inhibitor is to decrease the concentration of angiotensin-II, which lowers blood pressure, and to increase the concentration of bradykinin, which also lowers blood pressure. Figure 22.16 Regulation of vasoconstriction/vasodilation by angiotensin-II and bradykinin. The mechanism by which angiotensin-II stimulates vasoconstriction is shown in Figure 22.15. Angiotensin-converting enzyme is also responsible for bradykinin inactivation. Bradykinin stimulates endothelial cells to produce and secrete nitric oxide and prostacyclin, both of which are vasodilators. Consequently the effect of an ACE inhibitor is to decrease the concentration of angiotensin-II, which lowers blood pressure, and to increase the concentration of bradykinin, which also lowers blood pressure.
Mmg M, Stopka T, Julian BA, et al. Angiotensin II stimulates proliferation of normal early erythroid progenitors. J Clin Invest. Nov 1 1997 100(9) 2310-2314. [Pg.141]

Angiotensin II stimulates the influx of Ca" " into cardiac muscle cells and can exert a direct inotropic effect at cardiac muscle. In addition, angiotensin II can stimulate the sympathoadrenal system and thereby increase myocardial contractility. In contrast to its effects on vascular smooth muscle, the ability of angiotensin to increase the contractile force of the heart is far less potent. Therefore, in spite of the positive chronotropic and inotropic effects produced by angiotensin II, cardiac output is rarely increased. In fact, angiotensin II may decrease cardiac output through reflex bradycardia induced by the rise in peripheral resistance that it causes. In contrast, centrally administered angiotensin II increases both blood pressure and cardiac output. [Pg.209]

Angiotensin II stimulates aldosterone synthesis and secretion from the glomerulosa cells of the adrenal cortex. The aldosterone secretion induced by angiotensin II in humans is not accompanied by an increase in glucocorticoid plasma levels. Chronic administration of angiotensin II will maintain elevated aldosterone secretion for several days to weeks unless hypokalemia ensues. [Pg.210]

Berk, B. C., Vekshtein, V., Gordon, H. M., et al. 1989. Angiotensin II-stimulated protein synthesis in cultured vascular smooth muscle cells. Hypertension 13 305-314. [Pg.108]

Griendling, K. K., Minieri, C. A., Ollerenshaw, J. D., et al. 1994. Angiotensin II stimulates NADH and NADPH oxidase activity in cultured vascular smooth muscle cells. Circ Res 74 1141-1148. [Pg.109]

Leduc, I., and Meloche, S. 1995. Angiotensin II stimulates tyrosine phosphorylation of the focal adhesion-associated protein paxillin in aortic smooth muscle cells. J Biol Chem 270 4401 1404. [Pg.111]

Molloy, C. J., Taylor, D. S., and Weber, H. 1993. Angiotensin II stimulation of rapid protein tyrosine phosphorylation and protein kinase activation in rat aortic smooth muscle cells. J Biol Chem 268 7338-7345. [Pg.112]

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. [Pg.112]

Liao, D.F., Duff, J.L., Daum, G., Pelech, S.L., and Berk, B.C. 1996. Angiotensin II stimulates MAP kinase kinase kinase activity in vascular smooth muscle cells. Role of Raf. Circ Res 79 1007-1014. [Pg.206]

Gao BB, Hansen H, Chen HC, Feener EP. 2006. Angiotensin II stimulates phosphorylation of an ectodomain-truncated platelet-derived growth factor receptor-beta and its binding to class IA PI3K in vascular smooth muscle cells. Biochem J 397 337-344. [Pg.224]

Hama K, Ohnishi H, Yasuda H, Ueda N, Mashima H, Satoh Y, Hanatsuka K, Kita H, Ohashi A, Tamada K, Sugano K. 2004. Angiotensin II stimulates DNA synthesis of rat pancreatic stellate cells by activating ERK through EGF receptor transactivation. Biochem Biophys Res Commun 315 905-911. [Pg.225]

Li X, Lee JW, Graves LM, Earp HS. 1998. Angiotensin II stimulates ERK via two pathways in epithelial cells protein kinase C suppresses a G-protein coupled receptor-EGF receptor transactivation pathway. EMBO J 17 2574-2583. [Pg.226]

G. J. Bhat, T J. Thekkumkara, W.G. Thomas, K. M. Conrad, and K. M. Baker. Angiotensin II stimulates cis-inducing-fector-like DNA binding activity. J Biol Chem, 269, 31443-31449, 1994. [Pg.121]

NOTE Aldosterone production requires the renin-angiotension system Renin is an enzyme secreted by the juxtaglomerular ceils of the kidney in response to decreased arterial blood pressure and blood flow. Renin stimulates conversion of the protein angiotensinogen to angiotensin I which then becomes angiotensin II. Angiotensin II stimulates the synthesis and release of aldosterone by the adrenal cortex. [Pg.46]


See other pages where Angiotensin II stimulation is mentioned: [Pg.172]    [Pg.1067]    [Pg.396]    [Pg.35]    [Pg.726]    [Pg.727]    [Pg.728]    [Pg.330]    [Pg.141]    [Pg.727]    [Pg.728]    [Pg.729]    [Pg.60]    [Pg.298]    [Pg.75]    [Pg.266]    [Pg.100]    [Pg.135]    [Pg.136]    [Pg.121]    [Pg.192]    [Pg.205]    [Pg.162]    [Pg.45]    [Pg.156]    [Pg.1067]    [Pg.708]   
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