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Angiotensin-induced hypertension

Reckelhoff JF, Romero JC. 2003. Role of oxidative stress in angiotensin-induced hypertension. Am J Physiol 284 R893-912. [Pg.213]

Central nervous system. The existence of a central mechanism in angiotensin induced hypertension was first described by Bicker-ton and Buckley who have postulated its relation with norepinephrine action as central neurotransmitter. Recently it has been demonstrated by Palal c and Khairallah that angiotensin reduces up -take of -norepinephrine by rat brain,... [Pg.498]

Particularly when androgens/anabolics are misused to promote extreme muscular development, there is a risk of cardiomegaly and ultimate cardiac failure. Androgen-induced hypertension may be due to a hypertensive shift in the pressure-natriuresis relation, either by an increase in proximal tubular reabsorption or by activation of the renin-angiotensin system (27). This effect is not related to higher doses or longer treatment and can develop after a few months but can also be delayed for many years. [Pg.139]

Burke SL, Evans RG, Moretti JL, Head GA. Levels of renal and extrarenal sympathetic drive in angiotensin Il-induced hypertension. Hypertension. 2008 51 878-883. [Pg.78]

Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats. Fig. 1.7 Possible mechanisms involving angiotensin II, oxidative stress and nitric oxide in enhanced Gi oc protein expression in hypertension. Gi protein expression is enhanced in genetic (SHR) and experimental hypertension including 1 kidney 1 clip (1K1C) and L-NAME-induced hypertension. Inhibition of nitric oxide synthase (NOS) by L-NAME activates renin angiotensin system, and also decreases the level of NO. 1K1C hypertensive rats also exhibit enhanced levels of Ang II. Ang II increases oxidative stress that through increased MAP kinase activity results in enhanced expression of Gi oc proteins and thereby hypertension. On the other hand, increased levels of NO and cGMP decrease the expression of Gia proteins in VSMC which may be an additional mechanism through which NO decreases blood pressure in L-NAME-induced hypertensive rats.
Ichihara, S., Senbonmatsu, T., Price, E., Jr., et al. 2001. Angiotensin II type 2 receptor is essential for left ventricular hypertrophy and cardiac fibrosis in chronic angiotensin II-induced hypertension. Circulation 104 346-351. [Pg.110]

Weiss, D., Kools, J. J., and Taylor, W. R. 2001. Angiotensin Il-induced hypertension accelerates the development of atherosclerosis in apoE-deficient mice. Circulation 103 448-454. [Pg.114]

Zhang, Y., Griendling, K. K., Dikalova, A., et al. 2005c. Vascular hypertrophy in angiotensin II-induced hypertension is mediated by vascular smooth muscle cell-derived H2O2. Hypertension 46 732-737. [Pg.116]

Diep, Q.N., El Mabrouk, M., Yue, P., and Schiffrin, E.L. 2002. Effect of ATi receptor blockade on cardiac apoptosis in angiotensin Il-induced hypertension. Am. J. Physiol. 282 H1635-H1641. [Pg.133]

Mazzolai, L., Nussberger, J., Aubert, J.F., Brunner, D.B., Gabbiani, G., Bruner, H.R., and Pedrazzini, T. 1998. Blood pressure-independent cardiac hypertrophy induced by locally activated renin-angiotensin system. Hypertension 31 1324-1330. [Pg.245]

Sarr, M., Chataigneau, M., Martins, S., Schott, C., El Bedoui, J., Oak, M. H., Muller, B., Chataigneau, T., Schini-Keith, V. B. (2006). Red wine polyphenols prevent angiotensin 11-induced hypertension and endothelial dysfunction in rats role of NADPH oxidase. Cardiovasc. Res., 71, 794-802. [Pg.589]

The pathophysiology of ciclosporin-induced hypertension is complex and not yet fully elucidated. Increased systemic vascular resistance subsequent to altered vascular endothelium function, renal vasoconstriction with reduced glomerular filtration and sodium-water retention, and/or increased activity of the sympathetic nervous system were suggested, while only a minor role or none was attributed to the renin-angiotensin system (10). However, hypertension often occurs before changes in renal function or sodium balance can be demonstrated, and ciclosporin nephrotoxicity alone does not explain ciclosporin-associated hypertension (8,11). [Pg.744]

Ichihara A, Imig JD, Navar LG Neuronal nitric oxide synthase-dependent afferent arteriolar function in angiotensin ll-induced hypertension. Hypertension 33 462-466,1999... [Pg.210]

Hori, K., Suzuki, M., Tanda, S., Saito, S., Shiozaki, S. and Zhang, Q.H. (1991) Fluctuation in tumour blood flow under normotension and the effect of angiotensin II induced hypertension. Jpn. J. Cancer Res. 82 1309-1316. [Pg.599]

Hori K, Suzuki M, Tanda S, Saito D, Shinozaki M, Zhang QH. Fluctuations in tumor blood flow under normotension and the effect of angiotensin Il-induced hypertension. Jpn J Cancer Res 1991 82 1309-1316. [Pg.117]

Diz, D.I., Baer, P.G. and Nasjletti, A. (1983). Angiotensin Il-induced hypertension in the rat. Effects on the plasma concentration, renal excretion, and tissue release of prostaglandins. ]. Clin. Invest., 72, 466-477... [Pg.171]

Bush E, Maeda N, Kuziel WA, et al. CC chemokine receptor 2 is required for macrophage infiltration and vascular hypertrophy in angiotensin H-induced hypertension. Hypertension 2000 36 360-363. [Pg.32]


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