The effect of ozone on blood pressure in DOCA-salt-induced hypertensive rats
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE, cilt.8, sa.8, ss.12783-12791, 2015 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 8 Sayı: 8
- Basım Tarihi: 2015
- Dergi Adı: INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.12783-12791
- Anahtar Kelimeler: DOCA-salt, hypertension, ozone, blood pressure, endothelin-1, NITRIC-OXIDE RELEASE, AIR-POLLUTION, ENDOTHELIN RECEPTORS, OXIDATIVE STRESS, MESSENGER-RNA, KIDNEYS, HEART, VASOCONSTRICTION, INFLAMMATION, STIMULATION
- Kütahya Sağlık Bilimleri Üniversitesi Adresli: Hayır
Özet
Background: Hypertension is a risk factor for the cardiovascular diseases. Ozone as a therapeutic agent for the treatment of several disorders. We aimed to observe the effects of ozone on the blood pressure in DOCA-salt hypertensive rats. Methods: Twenty three young Sprague Dawley male rats were divided into three groups; Control (C), Hypertension (H) and Hypertension + Ozone (HO). Hypertension was induced by injection of DOCA-salt (25 mg/kg, s. c.) twice weekly, 4 weeks, whereas intraperitoneal ozone was administered (1.1 mg/kg) for 10 days. Serum endothelin-1, nitric oxide and renin levels were measured with ELISA. Blood pressures were monitored using a tail cuff system. Endothelin-1, ET receptor A and ET receptor B mRNA expression in heart and vascular tissue were assessed by quantitative reverse transcription polymerase chain reaction. Results: Blood pressure, serum endothelin-1 and ET receptor A mRNA expression levels were increased in H group, whereas serum renin, nitric oxide and ET receptor B mRNA expression levels in the heart and vascular tissue decreased compared with C and HO groups, which were counteracted by ozone treatment. Conclusion: Ozone treatment decreases blood pressure and is effective in preventing the progression of hypertensive disease, the mechanisms of which are associated with anti-vasoconstrictor effects through reducing the levels of serum endothelin-1 and ET receptor A mRNA expression in the heart and vascular tissue.