Circulating purine compounds, uric acid, and xanthine oxidase/dehydrogenase relationship in essential hypertension and end stage renal disease

References

• Rostand SG. Is renal failure caused by primary hypertension? Why does the controversy continue? Nephrol Dial Transpl. 1998;13:3007–3010
   PubMedGoogle Scholar
• Bidani AK, Griffin KA. Pathophysiology of hypertensive renal damage. Implications for therapy. Hypertension. 2004;44:595–601
   PubMed Web of Science ®Google Scholar
• Madhaven S, Stockwell D, Cohen H, Alderman MH. Renal function during antihypertensive treatment. Lancet. 1995;345:749–751
   PubMed Web of Science ®Google Scholar
• Rostand SG, Brown G, Kirk K, Rutsky EA, Dustan HP. Renal insufficiency in treated essential hypertension. N Engl J Med. 1989;320:684–688
   PubMed Web of Science ®Google Scholar
• Brazy PC, Fitzwilliam JF. Progressive renal disease: role of race and antihypertensive medications. Kidney Int. 1990;37:1113–1119
   PubMed Web of Science ®Google Scholar
• Kanellis J, Nakagawa T, Herrera-Acosta J, Schreiner GF, Rodriguez-Iturbe B, Johnson RJ. A single pathway for the development of essential hypertension. Cardiol Rev. 2003;11:180–196
   PubMedGoogle Scholar
• Fields LE, Burt VL, Cutler JA, Hughes J, Roccella EJ, Sorlie P. The burden of adult hypertension in the United States 1999 to 2000. A rising tide. Hypertension. 2004;44:398–404
   PubMed Web of Science ®Google Scholar
• Nakagawa T, Mazzali M, Kang DH, et al. Hyperuricemia causes glomerular hypertrophy in the rat. Am J Nephrol. 2003;23:2–7
   PubMed Web of Science ®Google Scholar
• Johnson R, Segal MS, Srinivas T, et al. Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link? JASN. 2005;16(7):1909–1919
   Google Scholar
• Mazzali M, Hughes J, Kim YG, et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism. Hypertension. 2001;38:1101–1106
   PubMed Web of Science ®Google Scholar
• Sanchez-Lozada LG, Tapia E, Santamaria J, et al. Mild hyperuricemia induces vasoconstriction and maintains glomerular hypertension in normal and remnant kidney rats. Kidney Int. 2005;67:237–247
   PubMed Web of Science ®Google Scholar
• Pearson JD, Gordon JL. Vascular endothelial and smooth muscle cells in culture selectively release adenine nucleotides. Nature. 1979;281:384–386
   PubMed Web of Science ®Google Scholar
• Gordon JL. Extracellular ATP: effects, sources and fate. Biochem J. 1986;233:309–319
   PubMed Web of Science ®Google Scholar
• Borst M, Schrader J. Adenine nucleotide release from isolated perfused guinea pig hearts and extracellular formation of adenosine. Circ Res. 1991;68:797–806
   PubMedGoogle Scholar
• Coade S, Pearson J. Metabolism of adenine nucleotides in human blood. Circ Res. 1989;65:531–537
   PubMed Web of Science ®Google Scholar
• Vial C, Owen P, Opie LH, Posel D. Significance of release of adenosine triphosphate and adenosine induced by hypoxia or adrenaline in perfused rat heart. J Mol Cell Cardiol. 1987;19:187–197
   PubMedGoogle Scholar
• Bergfeld GR, Forrester T. Release of ATP from human erythrocytes in response to a brief period of hypoxia and hypercapnia. Cardiovasc Res. 1992;26:40–47
   PubMed Web of Science ®Google Scholar
• Bodin P, Burnstock G. ATP-stimulated release of ATP by human endothelial cells. J Cardiovasc Pharmacol. 1996;27:872–875
   PubMedGoogle Scholar
• Beigi R, Kobatake E, Aizawa M, Dubyak GR. Detection of local ATP release from activated platelets using cell surface-attached firefly luciferase. Am J Physiol. 1999;276:C267–C278
   PubMedGoogle Scholar
• Bodin P, Burnstock G. Increased release of ATP from endothelial cells during acute inflammation. Inflamm Res. 1998;47:351–354
   PubMed Web of Science ®Google Scholar
• Schwiebert LM, Rice WC, Kudlow BA, Taylor AL, Schwiebert EM. Extracellular ATP signaling and P2X nucleotide receptors in monolayers of primary human vascular endothelial cells. Am J Physiol. 2002;282:C289–C301
   Google Scholar
• North RA. Molecular physiology of P2X receptors. Physiol Rev. 2002;82:1013–1067
   PubMed Web of Science ®Google Scholar
• Ralevic V, Burnstock G. Receptors for purines and pyrimidines. Pharmacol Rev. 1998;50:413–492
   PubMed Web of Science ®Google Scholar
• Darius H, Stahl GL, Lefer AM. Pharmacological modulation of ATP release from isolated rat hearts in response to vasoconstrictor stimuli using a continuous flow technique. J Pharmacol Exp Ther. 1987;240:542–547
   PubMedGoogle Scholar
• Berry CE, Hare JM. Xanthine oxidoreductase and cardiovascular disease: molecular mechanisms and pathophysiological implications. J Physiol. 2004;16;555(Pt 3):589–606
   Google Scholar
• Pacher P, Nivorozhkin A, Szabo C. Therapeutic effects of xanthine oxidase inhibitors: renaissance half a century after the discovery of allopurinol. Pharmacol Rev. 2006;58(1):87–114
   PubMed Web of Science ®Google Scholar
• Zhang Z, Blake DR, Stevens CR, et al. A reappraisal of xanthine dehydrogenase and oxidase in hypoxic reperfusion injury: the role of NADH as an electron donor. Free Radic Res. 1998;28(2):151–164
   PubMed Web of Science ®Google Scholar
• Spiekermann S, Landmesser U, Dikalov S, et al. Electron spin resonance characterization of vascular xanthine and NAD(P)H oxidase activity in patients with coronary artery disease: relation to endothelium-dependent vasodilation. Circulation. 2003;107(10):1383–1389
   PubMedGoogle Scholar
• de Jong JW, Schoemaker RG, de Jonge R, et al. Enhanced expression and activity of xanthine oxidoreductase in the failing heart. J Mol Cell Cardiol. 2000;32(11):2083–2089
   PubMedGoogle Scholar
• Pfeffer KD, Huecksteadt TP, Hoidal JR. Xanthine dehydrogenase and xanthine oxidase activity and gene expression in renal epithelial cells. Cytokine and steroid regulation. J Immunol. 1994;153(4):1789–1797
   PubMedGoogle Scholar
• National Kidney Foundation—K/DOQI. Clinical practice guidelines for chronic kidney disease: evaluation, classification and stratification. Am J Kidney Dis. 2002;39( suppl. 1):S1–S266
   PubMedGoogle Scholar
• Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The sixth report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure (JNC VI). Arch Intern Med. 1997;157:2413–2446
   PubMed Web of Science ®Google Scholar
• Coolen E, Arts I, Swennen E, Bast A, Cohen Stuart M, Dagnelie P. Simultaneous determination of adenosine triphosphate and its metabolites in human whole blood by RP-HPLC and UV-detection. J Chromatogr B. 2008;64:43–51
   Google Scholar
• Kizaki H, Sakurada T. Simple micro-assay methods for enzymes of purine metabolism. J Lab Clin Med. 1977;89(5):1135–1144
   PubMedGoogle Scholar
• Perneger TV, Nieto J, Whelton PK, Klag MJ, Comstock GW, Szklo M. A prospective study of blood pressure and serum creatinine. Results from the “Clue” study and the ARIC study. JAMA. 1993;269:488–493
   PubMed Web of Science ®Google Scholar
• Haroun MK, Jaar BG, Hoffman SC, Comstock GW, Klag MJ, Coresh J. Risk factors for chronic kidney disease: a prospective study of 25,534 men and women in Washington County, Maryland. J Am Soc Nephrol. 2003;14:2394–2441
   Google Scholar
• Lindeman RD, Tobin JD, Shock NW. Hypertension and the kidney. Nephron. 1989;47(Suppl. 1):62–67
   Google Scholar
• Goldbeter A. Modulation of the adenylate energy charge by sustained metabolic oscillations. FEBS Lett. 1974;43(3):327–330
   PubMedGoogle Scholar
• Tykarski A, Głuszek J, Banaszak F. Value of oxypurines and uric acid in plasma, renal excretion of oxypurines and uric acid as well as plasma adenosine deaminase and AMP deaminase activity in patients with essential hypertension. Pol Arch Med Wewn. 1993;89(3):223–229
   PubMedGoogle Scholar
• Kinugawa T, Ogino K, Osaki S, et al. Altered purine nucleotide degradation during exercise in patients with essential hypertension. Metabolism. 2001;50(6):646–650
   PubMedGoogle Scholar
• Romero JC, Reckelhoff JF. State-of-the-Art lecture: role of angiotensin and oxidative stress in essential hypertension. Hypertension. 1999;34:943–949
   PubMed Web of Science ®Google Scholar
• Watanabe S, Kang DH, Feng L, et al. Uric acid, hominoid evolution, and the pathogenesis of salt-sensitivity. Hypertension. 2002;40:355–360
   PubMedGoogle Scholar
• Johnson RJ, Srinivas T, Cade JR, Rideout BA, Oliver WJ. Uric acid, evolution and primitive cultures. Semin Nephrol. 2005;25:3–8
   PubMed Web of Science ®Google Scholar
• Graham A, McLees A, Kennedy C, Gould GW, Plevin R. Stimulation by the nucleotides, ATP and UTP of mitogen-activated protein kinase in EAhy 926 endothelial cells. Br J Pharmacol. 1996;117:1341–1347
   PubMedGoogle Scholar
• Kolosova IA, Mirzapoiazova T, Adyshev D, et al. Signaling pathways involved in adenosine triphosphate-induced endothelial cell barrier enhancement. Circ Res. 2005;97:115–124
   PubMedGoogle Scholar
• Patel V, Brown C, Goodwin A, Wilkie N, Boarder MR. Phosphorylation and activation of p42 and p44 mitogen-activated protein kinase are required for the P2 purinoceptor stimulation of endothelial prostacyclin production. Biochem J. 1996;320:221–226
   PubMedGoogle Scholar
• Bogatcheva NV, Dudek SM, Garcia JG, Verin AD. Mitogen-activated protein kinases in endothelial pathophysiology. J Investig Med. 2003;51:341–352
   PubMed Web of Science ®Google Scholar
• Lerman LO, Nath KA, Rodriguez-Porcel M, et al. Increased oxidative stress in experimental renovascular hypertension. Hypertension. 2001;37:541–546
   PubMed Web of Science ®Google Scholar