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By Robert W. Schrier

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Curr Opinion Nephrol Hypertens 1995, 4:416–420. 31. : Selective ADHinduced hypertrophy of the medullary thick ascending limb in Brattleboro rats. Kidney Int 1985, 28:456–466. 32. Chabardès D, Gagnan-Brunette M, Imbert-Tébol M: Adenylate cyclase responsiveness to hormones in various portions of the human nephron. J Clin Invest 1980, 65:439–448. 33. Stokes JB: Effects of prostaglandin E2 on chloride transport across the rabbit thick ascending limb of Henle. J Clin Invest 1979, 64:495–502. 34. Escalante B, Erlij D, Falck JR, McGiff JC: Effect of cytochrome P450 arachidonate metabolites on ion transport in rabbit kidney loop of Henle.

27. Barrett T, Bundey S: Wolfram (DIDMOAD) syndrome. J Med Genet 1997, 29:1237. 28. Holtzman EJ, Ausiello DA: Nephrogenic Diabetes insipidus: Causes revealed. Hosp Pract 1994, Mar 15:89–104. 29. Bichet D, Oksche A, Rosenthal W: Congential Nephrogenic Diabetes Insipidus. J Am Soc Nephrol 1997, 8:1951. 30. : Patients with autosomal nephrogenic diabetes insipidus homozygous for mutations in the aquaporin 2 water channel. Am J Hum Genet 1994, 55:648. 31. : Identification and characterization of aquaporin-2 water channel mutations causing nephrogenic diabetes insipidus with partial vasopressin response.

The inset shows this relation between mean arterial pressure (MAP), renal volume, and sodium excretion [4]. The effects of acute increases in arterial pressure on urinary excretion are shown by the solid curve. The chronic effects are shown by the dotted curve; note that the dotted line is identical to the curve in Figure 2-3. Thus, when the MAP increases, urinary output increases, leading to decreased ECF volume and return to the original pressure set point. UNaV—urinary sodium excretion volume.

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Atlas Of Diseases Of The Kidney by Robert W. Schrier

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