References
Liddle G.W., Bledsoe T., Coppage W.S. A familial renal disorder simulating primary aldosteronism but with negligible aldosterone secretion. Trans. Assoc. Am. Physicians 76: 199, 1963.
Botero-Velez M., Curtis J.J., Warnock D.G. Liddle’s syndrome revisited — A disorder of sodium reabsorption in the distal tubule. New. Engl. J. Med. 330: 178, 1994.
Canessa C.M., Schild L., Buell G., Thorens B., Gantschi I., Horisberger J.D., Rossier B. Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits. Nature 367: 463, 1994.
Shimkets R.A., Warnock D.G., Bositis C.M., Nelson-Williams C., Hansson J.H., Schambelan M., Gill J.R., Ulick S., Milora R.V., Findling J.W., Canessa C., Rossier B.C., Lifton R.P. Liddle’s syndrome: Heritable human hypertension caused by mutations in the ß subunit of the epithelial sodium channel. Cell. 79: 407, 1994.
Schild L., Canessa C.M., Shimkets R.A., Gautsch I., Lifton R.P., Rossier B.C. A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in xenopus laevis oocyte expression system. Proc. Natl. Acad. Sci. USA 92: 5699, 1995.
Lifton R.P., Dluhy R.G., Powers M., Rich G.M., Cook S., Ulick S., Lalouel J.M. A chimaeric 11ß-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension. Nature 355: 262, 1992.
Volpe M., Lembo G., De Luca M., Lamenza F., Tritto C., Ricciaderli B., Molaro M., De Campera P., Condorelli G., Rendina V., Trimarco B., Condorelli M. Abnormal hormonal and renal responses to saline load in hypertensive patients with parental history of cardiovascular accidents. Circulation. 84: 92, 1991.
Nabika T., Bonnardeaux A., James M., Julier C., Jeunemaitre X., Corvol P., Lathrop M., Soubrier F. Evaluation of the SA locus in human hypertension. Hypertension 25: 6, 1995.
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Shimkets, R.A., Warnock, D.G., Bositis, C.M. et al. Liddle’s syndrome: Heritable human hypertension caused by mutations in the ß subnit of the epithelial sodium channel. J Endocrinol Invest 18, 592–594 (1995). https://doi.org/10.1007/BF03349775
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DOI: https://doi.org/10.1007/BF03349775