Losartan ve Lizinoprilin Sıçan Torasik Aort Kasılmaları Üzerindeki Etkilerinde Siklooksijenaz Enzimlerinin Rolü

Amaç: Siklooksijenaz (COX) enzimleri tarafından sentezlenen prostaglandinlerin anjiotensin dönüştürücü enzim (ADE) inhibisyonu ve anjiotensin AT1 reseptör antagonizmasının etkilerine katkıda bulunduğu ve ADE sinyal yolakları ile COX enzimleri arasında etkileşme olduğu ileri sürülmüştür. Bu çalışmada anjiotensin II (Ang II) reseptör antagonisti bir ilaç olan losartan veya ADE inhibitörü bir ilaç olan lizinoprilin izole organ banyosunda sıçan torasik aorta kasılmaları üzerindeki etkilerinde COX enzimlerinin rolünün araştırılmasını amaçladık. Gereç ve Yöntem: Losartan (10-6,10-5,10-4M), lizinopril (10-6,10-5,10-4M) ve selektif olmayan bir COX inhibitörü olan dipironun (10-4,7x10-4,2x10-3M) tek başına fenilefrin (Phe) (10-7M), potasyum klorür (KCl) (6x10-2M) ve Ang II (10-8M) ile indüklenen kasılmalar üzerindeki ve ayrıca losartan veya lizinoprilin dipironla kombinasyonlarının Phe veya KCl ile indüklenen kasılmalar üzerindeki yanıtları kaydedildi. Bulgular: Tek başlarına verildiklerinde dipiron ve losartan Phe, KCl ve Ang II ile indüklenen kasılmaları baskılarken, lizinopril sadece Phe ve Ang II ile indüklenen kasılmaları baskıladı. COX enzimlerinin inhibisyonu (dipiron 10-4,7x10-4,2x10-3M tarafından sırasıyla COX-3, COX-3+-1, COX1+-2+3), losartan veya lizinoprilin gevşetici etkilerini artırdı. Ayrıca dipiron, lizinoprilin KCl ile indüklenen kasılmalar üzerindeki etkisini potansiyalize etti. Sonuç: Dipironun losartan veya lizinoprilin düz kas gevşetici etkilerini artırdığını ve COX enzim inhibisyonunun bu gevşemede rolü olabileceğini ileri sürüyoruzObjective: It was suggested that prostaglandins which are synthesized by cyclooxygenase (COX) enzymes contribute to the actions of angiotensin-converting enzyme (ACE) inhibition and angiotensin AT1 receptor antagonism and there is an interaction between ACE signaling pathway and COX enzymes. We aim to investigate the role of COX enzymes in the effects of losartan, an angiotensin II (Ang II) receptor antagonist or lisinopril, an ACE inhibitor, on the contractions of rat thoracic aorta in isolated tissue bath. Materials and Methods: Responses of losartan (10-6, 10-5, 10-4 M), lisinopril (10-6, 10-5, 10-4 M), and non-selective COX inhibitor dipyrone (10-4, 7 × 10-4, 2 × 10-3 M) alone to the contractions induced by phenylephrine (Phe) (10-7 M), potassium chloride (KCl) (6 × 10-2 M), Ang II (10-8 M) and responses of losartan or lisinopril in combination with dipyrone to the contractions induced by Phe or KCl were recorded. Results: When used alone, dipyrone and losartan inhibited Phe, KCl, and Ang II-induced contractions, whereas lisinopril inhibited only Phe and Ang II-induced contractions. Inhibition of COX enzymes (COX-3, COX-3 + COX-1, COX-1+ COX-2 + COX-3 by dipyrone 10-4, 7 × 10-4, 2 × 10-3 M, respectively) augmented the relaxant effects of losartan or lisinopril. Also, dipyrone potentiated the effect of lisinopril on KCl-induced contractions. Conclusion: We suggest that dipyrone increases the smooth-muscle relaxing effects of losartan or lisinopril and that COX enzyme inhibition may have a role in the enhancement of this relaxatio

Interaction of Sertraline and Nimodipine on Some Behavioural Tests in Rats

Background. Intracellular calcium contributes to the development of affective disorders. Also, calcium channel inhibitors influence the activity of many neurotransmitters and exert antidepressant and anxiolytic properties

The Role of Cyclooxygenase Enzymes in the Effects of Losartan and Lisinopril on the Contractions of Rat Thoracic Aorta

WOS: 000399175500004PubMed ID: 28416926Objective: It was suggested that prostaglandins which are synthesized by cyclooxygenase (COX) enzymes contribute to the actions of angiotensin-converting enzyme (ACE) inhibition and angiotensin AT1 receptor antagonism and there is an interaction between ACE signaling pathway and COX enzymes. We aim to investigate the role of COX enzymes in the effects of losartan, an angiotensin II (Ang II) receptor antagonist or lisinopril, an ACE inhibitor, on the contractions of rat thoracic aorta in isolated tissue bath. Materials and Methods: Responses of losartan (10(-6), 10(-5), 10(-4) M), lisinopril (10(-6), 10(-5), 10(-4) M), and non-selective COX inhibitor dipyrone (10(-4), 7 x 10(-4), 2 x 10(-3) M) alone to the contractions induced by phenylephrine (Phe) (10(-7) M), potassium chloride (KCl) (6 x 10(-2) M), Ang II (10(-8) M) and responses of losartan or lisinopril in combination with dipyrone to the contractions induced by Phe or KCl were recorded. Results: When used alone, dipyrone and losartan inhibited Phe, KCl, and Ang II-induced contractions, whereas lisinopril inhibited only Phe and Ang II-induced contractions. Inhibition of COX enzymes (COX-3, COX-3 + COX-1, COX-1+ COX-2 + COX-3 by dipyrone 10(-4), 7 x 10(-4), 2 x 10(-3) M, respectively) augmented the relaxant effects of losartan or lisinopril. Also, dipyrone potentiated the effect of lisinopril on KCl-induced contractions. Conclusion: We suggest that dipyrone increases the smooth-muscle relaxing effects of losartan or lisinopril and that COX enzyme inhibition may have a role in the enhancement of this relaxation