Xanthine oxidase and adenosine deaminase activities of renal tissue in rats with hypertension induced by N sup omega nitro-L-arginine methyj ester
Hipertansiyon böbrek fonksiyonlarını negatif yönde değiştirebilir. Pürin metabolizması hipertansiyondan dolayı olan kan damarlarıdaki daralmadan ve artan kalp atım hacminden etkilenebilir. Nitrik oksit sentazın (NOS) N sup omega Nitro-L-Arjinin Metil Ester (L-NAME) ile inhibisyonu sıçanlarda hipertansiyona yol açar. Bu çalışmanın amacı NOS inhibisyonu sonrası sıçanlarda renal doku adenozin deaminaz (AD) ve ksantin oksidaz (XO) aktivitelerini araştırmaktı. Sıçanlar üç gruba ayrıldı; biri kontrol ve diğerleri 15 gün süreyle içme sularında 100 veya 500 mg/L L-NAME uygulanan çalışma gruplarıydı. Yukarda açıklanan uygulamanın sonunda, anesteziye edilen sıçanlarda karotid arter kanülasyonu yoluyla arteryel kan basınçları ölçüldü. Renal dokuda AD ve XO aktiviteleri ölçüldü. Sistolik kan basınçları L-NAME gruplarında anlamlı artiş gösterdi. L-NAME gruplarındaki XO aktivitesi, kontrol grubuyla karşılaştırıldığında anlamlı olarak artmıştı. AD aktiviteleri de L-NAME gruplarında artmış olmasına karşın, bu artış anlamlı bulunmadı. 100 mg ve 500 mg L-NAME grupları arasında XO ve AD aktiviteleri açısından anlamlı fark yoktu. Sonuçta, L-NAME ile indüklenen hipertansiyonun pürin nükleotidlerinde artışa neden olduğu kanısına vardık. Böylece, artmış XO ve AD enzim aktiviteleri sonucu birikmiş pürin nükleotidleri renal dokudan uzaklaştırılabilinir.
N sup omega nitro-L-arjinin metil ester ile indüklenen hipertansiyonlu sıçanların renal doku ksantin oksidaz ve adenozin deaminaz aktiviteleri
Hypertension may alter kidney functions negatively. Purine metabolism may be affected from constricted blood vessels and increased cardiac output, because of hypertension. Nitric oxide synthase (NOS) inhibition by N sup omega Nitro-L- Arginine Methyl Ester (L-NAMK) produces hypertension in rats. The aim of this study was to investigate adenosine deaminase (AD) and xanthine oxidase (XO) activities of renal tissue in rats after NOS inhibition. Rats were divided into three groups; one of them was control group and the others were study groups treated with 100 or 500 mg per liter L-NAME in drinking tap water for 15 days. After above-mentioned treatment, arterial blood pressure was measured via carotid artery cannula on anaesthetised rats. Activities of AD and XO were carried out in the renal tissue. Systolic blood pressures showed significant increase in both L-NAME groups. XO activities of L-NAME groups were increased significantly compared to control group. Increased AD activities were also observed in L-NAME groups but this increase did not reach statistical significance. There was no significant difference in XO and AD activities between 100 mg and 500 mg L-NAME groups. In conclusion, we speculated that hypertension induced by L-NAME causes increased purine nucleotides. Then, accumulated purine nucleotides may be removed from the renal tissue by increased XO and AD enzyme activities.
___
- 1. Lacy 1', Gough DA, Sclimid-Schonbein GW. Role of xanthine oxidase in hydrogen peroxide production. Free Radic Biol Med 1998; 25: 720-727.
- 2. Parks DA, Granger DN. Xanthine oxidase: Biochemistry, distribution and physiology. Acra Physiol Sand 1986; 548: 87-99.
- 3. Cristalli G, Costanzi S, Lambertucci C, Lupidi G, Vittori S, Volpini R, Camaioni E. Adcnosine deaminase: functional implications and different classes of inhibitors. Med Res Rev 2001; 21: 105-128.
- 4. Moncada S. Nitric oxide in the vasculature: physiology and pathophysiology. Ann N V Acad Sci 1997; 811: 60-69.
- 5. Palmer RM, Ashton DS, Moncada S. Vascular endofjielial cells synthesize nitric oxide from L-arginine. Nature 1988; 333: 664-666. 6. Doggrell SA, Brown L. Rat models of hypertension, cardiac hypertrophy and failure. Cardiovasc Res 1998; 39: 89-105.
- 7. Jover B, Mimran A. Nitric oxide inhibition and renal alterations. J Cardiovasc Pharmacol 2001; 38 Suppl 2: S65-70.
- 8. Irmak MK, Koltuksuz U, Kutlu NO, Yağmurca M, Ozyurt H, Karaman A, Akyol O. The effect of caffeic acid phenethyl ester on ischemia-reperfusion injury in comparison with alpha-tocopherol in rat kidneys. Urol Res 2001; 29: 190-193.
- 9. Lowry O, Rosenbraugh N, Farr L, Rondall R. Protein measurement with the folin-phenol reagent. J Biol Chem 1951; 183: 265-275.
- 10. Giusti G. Adenosine deaminase; in Bergmeyer MV (ed): Methods of Enzymatic Analysis. 2'"1 ed. New York, Academic Press 1974: 1092-1098.
- 11. Prajda N, Weber G. Malign transformation-linked imbalance: decreased XO activity in hepatomas. FEBS Lett 1975; 59: 245-249. 12. Vural P. Nitric qxide/endothelin-1 in precclampsia. Clin Chim Acta 2002; 317:65 70.
- 13. Bergamaschi CT, Biancardi VC, Lopes OU, Campos RR. Effects of angiotensin blockade in the rostral ventrolateral medulla on maintenance of hypertension induced by chronic L-NAME treatment. Brain Res 2002; 927: 195-199.
- 14. Yoneyama T, Ohkawa S, Watanabe T, Odamaki M, Kumagai H, Kimura M, Hishida A. The contribution of nitric oxide to renal vascular wall thickening in rats with L-NAME-induced hypertension. Virchows Arch 1998; 433: 549-57.
- 15. Laakso J, Vaskonen T, Mervaala E, Vapaatalo H, Lapatto R. Inhibition of nitric oxide synthase induces renal xanthine oxidoreductase activity in spontaneously hypertensive rats. Life Sci 1999; 65: 2679-2685.
- 16. Jackson EK, Ohnishi A. Development and application of a simple microassay fo adenosine in rat plasma. Hypertension 1987; 10: 189-197.
- 17. Kuan CJ, Wells JN, Jackson EK. Endogenous adenosine restrains renin release in conscious rats. Circ Res 1990; 66: 637-646.
- 18. Tofovic SP, Kusaka H, Li P, Jackson EK. Effects of adenosine deaminase inhibition on blood pressure in old spontaneously hypertensive rats. Clin Exp Hypertens 1998; 20: 329-344. 19. Miguchi Y, Ono K, Sekita S, Onodera H, Mitsumori K, Nara Y, Satake M. Preventive effects of Shichimotsu-koka-to on renal lesions in stroke-prone spontaneously hypertensive rats. Biol Pharm Bull 1998; 21: 914-918.