Effect of quercetin on kinetic properties of renal Na,K-ATPase in normotensive and hypertensive rats

• Autorzy: Mezesova L. , Bartekova M. , Javorkova V. , Vlkovicova J. , Breier A. , Vrbjar N.
• Języki publikacji: EN

Abstrakty

EN

The effect of quercetin, a plant-derived bioflavonoid with documented positive effect on the cardiovascular system, was examined after 4-week supplementation in the dose of 20 mg kg-1·day-1 to young male normotensive control (C) and to spontaneously hypertensive rats (SHR) over the period of their 5th-8th week of age. The study was focused on the influence of quercetin on properties of the renal Na,K-ATPase, a key system in maintaining the homeostasis of sodium in the organism. Spontaneous hypertension by itself enhanced the activity of Na,K-ATPase probably as a consequence of a higher number of active enzyme molecules, as suggested by the 15% increase of Vmax, along with improved affinity to ATP, as indicated by the 30% decrease in the value of Michaelis-Menten constant Km in untreated SHR vs. untreated normotensive rats. Quercetin induced a decrease of Na,K-ATPase activity in the presence of all ATP and Na+ concentrations investigated. Evaluation of kinetic parameters resulted in a constant Vmax value. The ATP-binding properties of the enzyme were not influenced by quercetin, as suggested by statistically insignificant changes in the value of Km both in controls and in SHR. On the other hand, the affinity to sodium decreased, as suggested by an increase in the KNa value by 22% and 31% in normotensive and hypertensive groups, respectively. This impairment in the affinity of the Na+-binding site of Na,K-ATPase molecules was probably responsible for the deteriorated enzyme function in the kidneys of quercetin treated animals.

Słowa kluczowe

EN

bioflavonoids; cardiovascular system; enzyme; homeostasis; hypertension; kidney; kinetic property; normotension; quercetin; rat; sodium

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2010
• Tom: 61
• Numer: 5
• Opis fizyczny: p.593-598,fig.,ref.

Twórcy

autor

Mezesova L.

• Slovak Academy of Sciences, 9 Dubravska cesta Street, 840 05 Bratislava 45, P.O. Box 104, Slovak Republic

autor

Bartekova M.

autor

Javorkova V.

autor

Vlkovicova J.

autor

Breier A.

autor

Vrbjar N.

Bibliografia

• Renaud S, de Lorgeril M. Wine, alcohol, platelets and the French paradox for coronary heart disease. Lancet 1992; 339: 1523-1526.
• Hertog MG, Feskens EJ, Hollman PC, Katan MB, Kromhout D. Dietary antioxidant flavonoids and risk of coronary heart disease: the Zutphen Elderly Study. Lancet 1993; 342: 1007-1011.
• Terao J, Kawai Y, Murota K. Vegetable flavonoids and cardiovascular disease. Asia Pac J Clin Nutr 2008; 17: 291-293.
• Ossola B, Kaariainen TM, Mannisto PT. The multiple faces of quercetin in neuroprotection. Expert Opin Drug Saf 2009; 8: 397-409.
• Han JJ, Hao J, Kim CH, Hong JS, Ahn HY, Lee YS. Quercetin prevents cardiac hypertrophy induced by pressure overload in rats. J Vet Med Sci 2009; 71: 737-743.
• Becerra-Torres SL, Rodriguez-Vazquez ML, Medina-Ramirez IE, Jaramillo-Juarez F. The flavonoid quercetin protects and prevents against potassium dichromate-induced systemic peroxidation of lipids and diminution in renal clearance of para-aminohippuric acid and inulin in the rat. Drug Chem Toxicol 2009; 32: 88-91.
• Robak J, Gryglewski JR. Flavonoids are scavengers of superoxide anions. Biochem Pharmacol 1988; 37: 837-841.
• Duarte J, Andriambeloson E, Diebolt M, Andriantsitohaina R. Wine polyphenols stimulate superoxide anion production to promote calcium signalling and endothelial-dependent vasodilatation. Physiol Res 2004; 53: 595-602.
• Romero M, Jimenez R, Sanchez M, et al. Quercetin inhibits vascular superoxide production induced by endothelin-1: role of NADPH oxidase, uncoupled eNOS and PKC. Atherosclerosis 2009; 202: 58-67.
• Bartekova M, Ditte Z, Sulova Z, et al. The effect of quercetin on physiological and biochemical parameters of normotensive and hypertensive rats. Physiol Res 2008; 57: 9P.
• Egert S, Bosy-Westphal A, Seiberl J, et al. Quercetin reduces systolic blood pressure and plasma oxidised low-density lipoprotein concentrations in overweight subjects with a high-cardiovascular disease risk phenotype: a double-blinded, placebo-controlled cross-over study. Br J Nutr 2009; 102: 1065-1074.
• Perez-Vizcaino F, Duarte J, Jimenez R, Santos-Buelga C, Osuna A. Antihypertensive effects of the flavonoid quercetin. Pharmacol Rep 2009; 61: 67-75.
• Pei TX, Xu CQ, Li B, et al. Protective effect of quercetin against adriamycin-induced cardiotoxicity and its mechanism in mice. Yao Xue Xue Bao 2007; 42: 1029-1033.
• Shoshan V, Campbell KP, MacLennan DH, Frodis W, Britt BA. Quercetin inhibits Ca2+ uptake but not Ca2+ release by sarcoplasmic reticulum in skinned muscle fibers. Proc Natl Acad Sci USA 1980; 77: 4435-4438.
• McKenna E, Smith JS, Coll KE, et al. Dissociation of phospholamban regulation of cardiac sarcoplasmic reticulum Ca21ATPase by quercetin. J Biol Chem 1996; 271: 24517-24525.
• Kuriki Y, Racker E. Inhibition of (Na+,K+)adenosine triphosphatase and its partial reactions by quercetin. Biochemistry 1976; 15: 4951-4956.
• Robinson JD, Robinson LJ, Martin NJ. Effects of oligomycin and quercetin on the hydrolytic activities of the (Na+/K+)-dependent ATPase. Biochim Biophys Acta 1984; 772: 295-306.
• Zheng J, Ramirez VD. Inhibition of mitochondrial proton F0F1-ATPase/ATP synthase by polyphenolic phytochemicals. Br J Pharmacol 2000; 130: 1115-1123.
• Gasparin FR, Spitzner FL, Ishii-Iwamoto EL, Bracht A, Constantin J. Actions of quercetin on gluconeogenesis and glycolysis in rat liver. Xenobiotica 2003; 33: 903-911.
• Jorgensen PL, Pedersen PA. Structure-function relationships of Na, K, ATP, or Mg binding and energy transduction in Na,K-ATPase. Biochim Biophys Acta 2001; 1505: 57-74.
• Melzi ML, Bertorello A, Fukunda Y, Muldin I, Sereni F, Aperia A. Na, K-ATPase activity in renal tubule cells from Milan hypertensive rats. Am J Hypertens 1989; 2: 563-566.
• Ikari A, Tachihara Y, Kawano K, Suketa Y. Differential regulation of Na+,K+-ATPase and the Na+-coupled glucose transporter in hypertensive rat kidney. Biochim Biophys Acta 2001; 1510: 118-124.
• Jorgensen PL. Purification and characterization of Na+,K+-ATPase: III. Purification from the outer medulla of mammalian kidney after selective removal of membrane components by sodium dodecylsulphate. Biochim Biophys Acta 1974; 356: 36-52.
• Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the folin phenol reagent. J Biol Chem 1951; 193: 265-275.
• Taussky HH, Shorr EE. A microcolorimetric method for the determination of inorganic phosphorus. J Biol Chem 1953; 202: 675-285.
• Edmondson RP, Thomas RD, Hilton PJ, Patrick J, Jones NF. Abnormal leukocyte composition and sodium transport in essential hypertension. Lancet 1975; 1: 1003-1005.
• Ambresioni E, Costa FV, Montebugnoli L, Tartagni F, Magnani B. Increased intralymphocytic sodium content in essential hypertension: an index of impaired sodium cellular metabolism. Clin Sci 1981; 61: 181-186.
• Haddy FJ. Digitalislike circulating factor in hypertension: potential messenger between salt balance and intracellular sodium. Cardiovasc Drugs Ther 1990; 4: 343-349.
• de Wardener HE, MacGregor GA. The relation of a circulating sodium transport inhibitor (the natriuretic hormone?) to hypertension. Medicine (Baltimore) 1983; 62: 310-326.
• Cooper RS, Shamsi N, Katz S. Intracellular calcium and sodium in hypertensive patients. Hypertension (Dallas) 1987; 9: 224-229.
• Sudar E, Velebit J, Gluvic Z, et al. Hypothetical mechanism of sodium pump regulation by estradiol under primary hypertension. J Theor Biol 2008; 251: 584-592.
• Pamnani MB, Clough DL, Huot SJ, Haddy FJ. Sodium-potassium pump activity in experimental hypertension. In: Vasodilatation, P.M. Vanhoutte, I. Leusen, (eds.) New York, Raven Press, 1981, pp. 391-403.
• Pamnani M, Huot S, Buggy J, Clough D, Haddy F. Demonstration of a humoral inhibitor of the Na+-K+ pump in some models of experimental hypertension. Hypertension 1981; 3: 96-101.
• Clough DL, Pamnani MB, Haddy FJ. Myocardial Na,K-ATPase activity in rats with steroid and spontaneous hypertension. J Hypertens 1984; 2: 141-147.
• Vlkovicova J, Javorkova V, Pechanova O, Vrbjar N. Gender difference in functional properties of Na,K-ATPase in the heart of spontaneously hypertensive rats. Life Sci 2005; 76: 971-982.
• Javorkova V, Vlkovicova J, Kunes J, Pechanova O, Zicha J, Vrbjar N. Effect of maturation on renal Na+/K+-ATPase and its susceptibility to nitric oxide-deficient hypertension in rats. Clin Exp Pharmacol Physiol 2007; 34: 617-623.
• Javorkova V, Pechanova O, Andriantsitohaina R, Vrbjar N. Effect of polyphenolic compounds on the renal Na+,K+-ATPase during development and persistence of hypertension in rats. Exp Physiol 2004; 89: 73-81.
• Tsuruya Y, Ikeda U, Kawakami K, et al. Augmented Na,K-ATPase gene expression in spontaneously hypertensive rat hearts. Clin Exp Hypertens 1991; 13: 1213-222.
• Bartekova M, Carnicka S, Pancza D, Ondrejcakova M, Breier A, Ravingerova T. Acute treatment with polyphenol quercetin improves postischemic recovery of isolated perfused rat hearts after global ischemia. Can J Physiol Pharmacol 2010; 88: 465-471.
• Maneva A, Taleva B. Effect of some flavonic compounds and ascorbic acid on lactoferrin stimulation of erythrocyte glycolysis and Na+/K+-atpase activity. Z Naturforsch C 2008; 63: 773-779.
• de Boer VC, Dihal AA, van der Woude H, et al. Tissue distribution of quercetin in rats and pigs. J Nutr 2005; 135: 1718-1725.
• Bieger J, Cermak R, Blank R, et al. Tissue distribution of quercetin in pigs after long-term dietary supplementation. J Nutr 2008; 138: 1417-1420.
• Eldin AA, Shaheen AA, Abd Elgawad HM, Shehata NI. Protective effect of taurine and quercetin against renal dysfunction associated with the combined use of gentamycin and diclofenac. Indian J Biochem Biophys 2008; 45: 332-340.
• Vlkovicova J, Javorkova V, Mezesova L, Pechanova O, Andriantsitohaina R, Vrbjar N. Dual effect of polyphenolic compounds on cardiac Na+,K+-ATPase during development and persistance of hypertension in rats. Can J Physiol Pharmacol 2009; 87: 1046-1054.
• Javorkova V, Pechanova O, Andriantsitohaina R, Vrbjar N. Effect of polyphenolic compounds on the renal Na+,K+-ATPase during the restoration of normotension after experimentally induced hypertension in rats. Exp Physiol 2003; 88: 475-482.
• Andriambeloson E, Stoclet JC, Andriantsitohaina R. Mechanism of endothelial nitric oxide-dependent vasorelaxation induced by wine polyphenols in rat thoracic aorta. J Cardiovasc Pharmacol 1999; 33: 248-254.
• Orellana M, Araya J, Guajardo, Rodrigo R. Modulation of cytochrome P450 activity in the kidney of rats following long-term red wine exposure. Comp Biochem Physiol C 2002; 132: 399-405.
• Rodrigo R, Gonzalo R, Orellana M, Arya J, Bosco C. Rat kidney antioxidant response to long-term exposure to flavonol rich red wine. Life Sci 2002; 71: 2881-2895.
• Rodrigo R, Rivera G. Renal damage mediated by oxidative stress: a hypothesis of protective effects of red wine. Free Radic Biol Med 2002; 33: 409-422.
• Rodrigo R, Bosco C, Herrera P, Rivera G. Amelioration of myoglobinuric renal damage in rats by chronic exposure to flavonol-rich red wine. Nephrol Dial Transplant 2004; 19: 2237-2244.