The role of mineralocorticoid receptor antagonists in the treatment of cardiac failure

Bibliography

• FELDMAN D, FUNDER JVV, EDELMAN IS: Subcellular mechanisms in the action of adrenal steroids. Am. Med. (1972) 53:545–560.
   PubMed Web of Science ®Google Scholar
• KROZOWSKI ZS, FUNDER JVV: Renal mineralocorticoid receptors and hippocampal corticosterone binding species have identical intrinsic steroid specificity. Proc. Nati Acad. Sci. USA (1983) 80:6056–6060.
   PubMed Web of Science ®Google Scholar
• MYLES K, FUNDER JW: Type I (mineralocorticoid) receptors in the guinea-pig. Am. Physiol. (1994) 267:E268–E272.
   PubMed Web of Science ®Google Scholar
• ARRIZA JL, WEINBERGER C, CERELLI G et al.: Cloning of human mineralocorticoid receptor complementary DNA: structural and functional kinship with the glucocorticoid receptor. Science (1987) 237:268–275.
   PubMed Web of Science ®Google Scholar
• FUNDER JVV, PEARCE PT, SMITH R,SMITH Al: Mineralocorticoid action: target-tissue specificity is enzyme, not receptor, mediated. Science (1988) 242:583–585.
   PubMed Web of Science ®Google Scholar
• EDWARDS CR, STEWART PM, BURT D et al.: Localisation of 11 beta-hydroxysteroid dehydrogenase — tissue specific protector of the mineralocorticoid receptor. Lancet (1988) 29:986–989.
   Google Scholar
• WILSON RC, KROZOWSKI ZS, LI K et al.: A mutation in the HSD11B2 gene in a family with Apparent Mineralocorticoid excess. Clin. Endocrinol. Metab. (1995) 80:2263–2266.
   Google Scholar
• FUNDER JW, MYLES K: Exclusion of corticosterone from epithelial mineralocorticoid receptors is insufficient for selectivity of aldosterone action: in vivo binding studies. Endocrinology (1997) 137(12):5264–5268.
   Web of Science ®Google Scholar
• ••Shows that even in '1113-HSD2-protected'aldosterone target tissues most MR are occupied but normally not activated by glucocorticoids.
   Google Scholar
• FUNDER JW, BLAIR-WEST JR, COGHLAN JP, DENTON DA, SCOGGINS BA, WRIGHT RD: Effect of plasma (K+) on the secretion of aldosterone. Endocrinology (1969) 85:381–384.
   PubMed Web of Science ®Google Scholar
• OKUBO S, NIIMURA F, NISHIMURA H et al.: Angiotensin-independent mechanism for aldosterone synthesis during chronic extracellular fluid volume depletion. j Clin. Invest. (1997) 99:855–860.
   PubMed Web of Science ®Google Scholar
• BRILLA CG, WEBER KT: Mineralocorticoid excess, dietary sodium, and myocardial fibrosis. .1. Lab. Clin. Med. (1992) 120(6):893–901.
   Google Scholar
• ROCHA R, RUDOLPH AE, FRIERDICH GE: Aldosterone induces a vascular inflammatory phenotype in the rat heart. Am. .1 Physiol. (2002) 283:H1802–H1810.
   PubMed Web of Science ®Google Scholar
• ROCHA R, MARTIN-BERGER CL, YANG P: Selective aldosterone blockade prevents angiotensin II/salt-induced vascular inflammation in the rat heart. Endocrinology (2002) 143:4828–4836.
   PubMed Web of Science ®Google Scholar
• SELYE H, HALL CE, ROWLEY EM: Malignant hypertension produced by treatment with deoxycorticosterone acetate and sodium chloride. Can. Med. Assoc. (1943) 49:88–93.
   PubMedGoogle Scholar
• PITT B, ZANNAD F, REMME WJ et aL: The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators. N Engl. Med. (1999) 41:709–717.
   Google Scholar
• ••Demonstration of extraordinary benefits ofMR blockade in severe congestive cardiac failure.
   Google Scholar
• ZANNAD F, ALLA F, SOUSSET B, PEREZ A, PITT B: Limitation of excessive extracellular matrix turnover may contribute to survival benefit of spironolactone therapy in patients with congestive heart failure. Circulation (2000) 102(22):2700–2706.
   PubMed Web of Science ®Google Scholar
• PITT B, REMME W, ZANNAD F et al.:Eplerenone, a selective aldosterone blocker, in patients with left ventricular dysfunction after myocardial infarction. N Engl. I Med. (2003) 348(14):1309–1321.
   PubMed Web of Science ®Google Scholar
• ••Even in mild, post-myocardial infarct heartfailure, MR blockade with the selective antagonist eplerenone confers significant advantages in terms of mortality and hospitalisation.
   Google Scholar
• SUZUKI G, MORITA H, MISHIMA T et al.: Effects of long-term monotherapy with eplerenone, a novel aldosterone blocker, on progression of left ventricular dysfunction and remodeling in dogs with heart failure. Circulation (2002) 106(23):2967–2972.
   PubMed Web of Science ®Google Scholar
• QIN W, RUDOLPH AE, BOND BR et al: A transgenic model of aldosterone-driven cardiac hypertrophy and heart failure. Circ. Res. (2003) 93(1):69–76.
   PubMed Web of Science ®Google Scholar
• SUN Y, RATAJSKA A, WEBER KT: Inhibition of angiotensin converting enzyme and attenuation of myocardial fibrosis by lisinopril in rats receiving angiotensin 11.1 Lab. Clin. Med. (1995) 126:95–101.
   PubMedGoogle Scholar
• ROBERT V, SILVESTRE J-S, CHARLEMAGNE D et al.: Biological determinants of aldosterone-induced cardiac fibrosis in rats. Hypertension (1995) 26:971–978.
   PubMed Web of Science ®Google Scholar
• WARD MR, KANELLAKIS P, RAMSEY D, FUNDERJW, BOBIK A: Eplerenone suppresses constrictive remodeling and collagen accumulation after angioplasty in porcine coronary arteries. Circulation (2001) 104:467–472.
   PubMed Web of Science ®Google Scholar
• •MR blockade can block the fibrotic response to tissue injury even in the absence of elevated aldosterone/salt.
   Google Scholar
• ROCHA R, STIER CT Jr: Pathophysiological effects of aldosterone in cardiovascular tissues. Trends Endocrinol. Metab. (2001) 12(7):308–314.
   PubMed Web of Science ®Google Scholar
• STOWASSER M, GORDON RD, GUNASEKERA TG et al.: High rate of detection of primary aldosteronism, including surgically treatable forms, following 'non-selective' screening of hypertensives attending a recently established Hypertension Unit. I Hyperten. (2003) 21(11):2149–2157.
   PubMed Web of Science ®Google Scholar
• McKELVIE RS, YUSUF S, PERICAK D et al.: Comparison of candesartan, enalapril, and their combination in congestive heart failure: randomized evaluation of strategies for left ventricular dysfunction (RESOLVD) pilot study. The RESOLVD Pilot Study Investigators. Circulation (1999) 100(10):1056–1064.
   PubMed Web of Science ®Google Scholar
• COHN JN, TOGNONI G: A randomizedtrial of the angiotensin-receptor blocker valsartan in chronic heart failure. N Engl. Med. (2001) 345:1667–1675.
   PubMed Web of Science ®Google Scholar
• YOUNG MJ, MOUSSA L, DILLEY R, FUNDER JW: Early inflammatory responses in experimental cardiac hypertrophy and fibrosis: effects of 1113-hydroxysteroid dehydrogenase inactivation. Endocrinology (2003) 144(3):1121–1125.
   PubMed Web of Science ®Google Scholar
• •Vascular inflammatory effect of mineralocorticoids can be mimicked by carbenoxolone administration.
   Google Scholar
• FUNDER JW: Enzymes and receptors: challenges and future directions. Steroids (1994) 59:164–169.
   PubMed Web of Science ®Google Scholar
• KITAGAWA H, YANAGISAWA J, FUSE H et al.: Ligand-selective potentiation of rat mineralocorticoid receptor activation function 1 by a CBP-containing histone acetyltransferase complex. Mol. Cell Biol. (2002) 22:3698–3706.
   PubMed Web of Science ®Google Scholar
• •Demonstration of ligand-dependent differential cofactor binding by MR.
   Google Scholar
• GOMEZ-SANCHEZ EP, VENKATARAMAN MT, THWAITES D, FORT C: ICV infusion of corticosterone antagonizes ICV-aldosterone hypertension. Am. .1 Physiol. (1990) 258:E649–E653.
   Google Scholar
• SATO A, FUNDER JW: High glucose stimulates aldosterone-induced hypertrophy via Type I mineralocorticoid receptors in neonatal rat cardiomyocytes. Endocrinology (1996) 137(10):4145–4153.
   PubMed Web of Science ®Google Scholar
• ZHANG Q, PISTON DW, GOODMAN RH: Regulation of corepressor function by nuclear NADH. Science (2002) 295(5561):1895–1897.
   PubMed Web of Science ®Google Scholar
• FJELD CC, BIRDS ONG WT, GOODMAN RH: Differential binding of NAD± allows the transcriptional compressor carboxyl-terminal binding protein to serve as a metabolic sensor. Proc. Nati Acad. Sci. USA (2003) 100(16):9202–9207.
   PubMed Web of Science ®Google Scholar
• •Modification of transcription factor corepressor activity by NADH.
   Google Scholar