Hipertansiyon böbrek fonksiyonlarini negatif yönde degistirebilir. Pürin metobolizmasi hipertansiyondan dolayi
olan kan damarlaridaki daralmadan ve artan kalp atim hacminden etkilenebilir. Nitrik oksit sentazin (NOS) N sup
omega Nitro-L-Arjinin Metil Ester (L-NAME) ile inhibisyonu siçanlarda hipertansiyona yol açar. Bu çalismanin
amaci NOS inhibisyonu sonrasi siçanlarda renal doku adenozin deaminaz (AD) ve ksantin oksidaz (XO)
aktivitelerini arastirmakti. Siçanlar üç gruba ayrildi; biri kontrol ve digerleri 15 gün süreyle içme sularinda 100 veya
500 mg/L L-NAME uygulanan çalisma gruplariydi. Yukarda açiklanan uygulamanin sonunda, anesteziye edilen
siçanlarda karotid arter kanülasyonu yoluyla arteryel kan basinçlari ölçüldü. Renal dokuda AD ve XO aktiviteleri
ölçüldü.
Sistolik kan basinçlari L-NAME gruplarinda anlamli artis gösterdi. L-NAME gruplarindaki XO aktivitesi, kontrol
grubuyla karsilastirildiginda anlamli olarak artmisti. AD aktiviteleri de L-NAME gruplarinda artmis olmasina
karsin, bu artis anlamli bulunmadi. 100 mg ve 500 mg L-NAME gruplari arasinda XO ve AD aktiviteleri açisindan
anlamli fark yoktu.
Sonuçta, L-NAME ile indüklenen hipertansiyonun pürin nükleotidlerinde artisa neden oldugu kanisina vardik.
Böylece, artmis XO ve AD enzim aktiviteleri sonucu birikmis pürin nükleotidleri renal dokudan uzaklastirilabilinir.
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-NAME) 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.