« Previous
Next »
Journal of the American Society of Hypertension
Volume 2, Issue 5
, Pages 341-348
, September 2008
Reduced isoproterenol-induced renin-angiotensin changes and extracellular matrix deposition in hearts of TGR(A1–7)3292 rats
References
- . Role of intracardiac renin-angiotensin-aldosterone system in extracellular matrix remodeling. Methods Find Exp Clin Pharmacol. 2003;25:541–564
- . Pathological hypertrophy and cardiac interstitium (Fibrosis and renin-angiotensin-aldosterone system). Circulation. 1991;83:1849–1865
- Impairment of in vitro and in vivo heart function in angiotensin-(1–7) receptor Mas knockout mice. Hypertension. 2006;47:996–1002
- . Angiotensin-(1–7) and its receptor as a potential targets for new cardiovascular drugs. Expert Opin Investig Drugs. 2005;14:1019–1031
- . Angiotensin-(1–7): cardioprotective effect in myocardial ischemia/reperfusion. Hypertension. 2001;38:665–668
- Prevention of angiotensin II-induced cardiac remodeling by angiotensin-(1–7). Am J Physiol Heart Circ Physiol. 2007;292:H736–H742
- Angiotensin-(1–7) attenuates the development of heart failure after myocardial infarction in rats. Circulation. 2002;105:1548–1550
- The nonpeptide angiotensin-(1–7) receptor Mas agonist AVE 0991 attenuates heart failure induced by myocardial infarction. Am J Physiol Heart Circ Physiol. 2007;292:H1113–H1119
- . Angiotensin-(1–7) improves the post-ischemic function in isolated perfused rat hearts. Braz J Med Biol Res. 2002;35:1083–1090
- . Angiotensin-(1–7) inhibits growth of cardiac myocytes through activation of the Mas receptor. Am J Physiol Heart Circ Physiol. 2005;289:H1560–H1566
- Angiotensin-(1–7) is an endogenous ligand for the G protein-coupled receptor Mas. Proc Natl Acad Sci U S A. 2003;100:8258–8263
- Angiotensin-(1–7) binds to specific receptors on cardiac fibroblasts to initiate anti-fibrotic and anti-trophic effects. Am J Physiol Heart Circ Physiol. 2005;289:H2356–H2363
- . Effects of genetic deletion of angiotensin-(1–7) receptor Mas on cardiac function during ischemia/reperfusion in the isolated perfused mouse heart. Life Sci. 2006;80:264–268
- . Chronic angiotensin-(1–7) prevents cardiac fibrosis in DOCA-salt model of hypertension. Am J Physiol Heart Circ Physiol. 2006;290:H2417–H2423
- Expression of an angiotensin-(1–7)-producing fusion protein produces cardioprotective effects in rats. Physiol Genomics. 2004;17:292–299
- . Expression of an angiotensin-(1–7)-producing fusion protein in rats induced marked changes in regional vascular resistance. Am J Physiol Heart Circ Physiol. 2007;292:H2485–H2490
- . Plasma angiotensin-(1–7) immunoreactivity is increased by salt load, water deprivation, and hemorrhage. Peptides. 1994;15:723–729
- . A rapid and sensitive method for the quantification of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem. 1976;72:248–254
- . Angiotensin-(1–7) prevents development of severe hypertension and end-organ damage in spontaneously hypertensive rats treated with L-NAME. Am J Physiol Heart Circ Physiol. 2006;290:H684–H691
- ACE2 gene transfer attenuates hypertension-linked pathophysiological changes in the SHR. Physiol Genomics. 2006;27:12–19
- Isoproterenol-induced impairment of heart function and remodeling are attenuated by the nonpeptide angiotensin-(1–7) analogue AVE 0991. Life Sci. 2007;81:916–923
- . Interplay of angiotensin II and angiotensin-(1–7) in the regulations of matrix metalloproteinases of human cardiocytes. Exp Physiol. 2008;93:599–612
- . Chronic infusion of angiotensin-(1–7) reduces heart angiotensin II levels in rats. Regul Pept. 2005;125:29–34
- . Is angiotensin II a direct mediator of left ventricular hypertrophy? (Time for another look). Hypertension. 2007;49:1196–1201
- . Upregulation of angiotensin-converting enzyme 2 after myocardial infarction by blockade of angiotensin II receptors. Hypertension. 2004;43:970–976
- Enalapril attenuates downregulation of angiotensin-converting enzyme 2 in the late phase of ventricular dysfunction in myocardial infarcted rat. Hypertension. 2006;48:572–578
This work was supported by CNPq-PRONEX (Conselho Nacional de Desenvolvimento Científico e Tecnológico), FAPEMIG-PRONEX (Fundação de Amparo à Pesquisa de Minas Gerais), and CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior).
Conflict of interest: none.
PII: S1933-1711(08)00075-2
doi: 10.1016/j.jash.2008.04.012
© 2008 American Society of Hypertension. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Journal of the American Society of Hypertension
Volume 2, Issue 5
, Pages 341-348
, September 2008
