Browsing by Author "Ulus, Ismail Hakki"
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Item Central choline suppresses plasma renin response to graded haemorrhage in rats(Wiley, 2008-10) Işbil Büyükcoşkun, Naciye; İlçöl, Yeşim Özarda; Cansev, Mehmet; Hamurtekin, Emre; Özlük, Kasım; Ulus, Ismail Hakki; Uludağ Üniversitesi/Tıp Fakültesi/Fizyoloji Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Biyokimya Anabilim Dalı.; Uludağ Üniversitesi/Tıp Fakültesi/Klinik Farmakoloji Anabilim Dalı.; 0000-0003-2918-5064; AAL-8873-2021; M-9071-2019; D-5340-2015; AAH-1692-2021; 55665951400; 35741320500; 8872816100; 8717648500; 6602676331; 70042710861. Central administration of choline increases blood pressure in normotensive and hypotensive states by increasing plasma concentrations of vasopressin and catecholamines. We hypothesized that choline could also modulate the renin-angiotensin pathway, the third main pressor system in the body. 2. Plasma renin activity (PRA), which serves as an index of the function of the peripheral renin-angiotensin system, was determined in rats subjected to graded haemorrhage following central choline administration. 3. Intracerebroventricular (i.c.v.) injection of choline (12.5-150 mu g), a precursor of the neurotransmitter acetylcholine (ACh), inhibited the increase in PRA in rats subjected to graded haemorrhage by sequential removal of 0.55 mL blood/100 g bodyweight. Choline, in the range 50-150 mu g, increased blood pressure. 4. Intraperitoneal (i.p.) administration of 150 mu g choline failed to alter blood pressure and plasma renin responses to graded haemorrhage. Administration of a higher dose (90 mg/kg, i.p.) of choline decreased blood pressure and enhanced PRA in the first two blood samples obtained during the graded haemorrhage. Physostigmine (10 mu g, i.c.v.), ACh (10 mu g, i.c.v.), carbamylcholine (10 mu g, i.c.v.) and cytidine 5'-diphosphocholine (CDP-choline; 250 mu g, i.c.v.) increased blood pressure and attenuated plasma renin responses to graded haemorrhage. 5. Inhibition of PRA by i.c.v. choline was abolished by i.c.v. pretreatment with mecamylamine (50 mu g), but not atropine (10 mu g). Blood pressure responses to choline (150 mu g) were attenuated by pretreatment with both mecamylamine and atropine. 6. Inhibition of PRA in response to central choline administration was associated with enhanced plasma vasopressin and catecholamine responses to graded haemorrhage. Pretreatment of rats with a vasopressin antagonist reversed central choline-induced inhibition of plasma renin responses to graded haemorrhage without altering the blood pressure response. 7. In conclusion, central administration of choline inhibits the plasma renin response to graded haemorrhage. Nicotinic receptor activation and an increase in plasma vasopressin appear to be involved in this effect.Item Serum choline and butyrylcholinesterase changes in response to endotoxin in calves receiving intravenous choline administration(Elsevier, 2019-07-09) Eralp İnan, Oya; Tvarijonaviciute, Asta; Rubio, Camila Peres; Cerón, José Joaquín; Ulus, Ismail Hakki; Kocatürk, Meriç; Kasap, Sevim C.; Cansev, Mehmet; Yılmaz, Zeki; Uludağ Üniversitesi/Veteriner Fakültesi/İç Hastalıkları Anabilim Dalı; Uludağ Üniversitesi/Tıp Fakültesi/Farmakoloji Anabilim Dalı.; 0000-0002-2849-1222; 0000-0001-9836-0749; V-5578-2017; AAP-7998-2020; M-9071-2019; A-9637-2008; 36437200800; 36514844800; 8872816100; 35944810500Endotoxemia treatment options are still of interest due to high mortality and choline treatment is one of them because of its role in the cholinergic anti-inflammatory pathway. This study investigated serum choline and butyrylcholinesterase (BChE) responses, and their correlations with inflammatory, oxidative stress and tissue damage biomarkers, including paraoxanase-1 (PON1), and clinical signs in calves with endotoxemia and the effect of choline treatment in these responses. Healthy calves (n = 20) were divided equally into 4 groups: Control (0.9% NaCl, iv), Choline (C; 1 mg/kg/iv,once), Lipopolysaccharide (LPS; 2 mu g/kg/iv,once) and LPS + C. Clinical and laboratory examinations were performed before and 0.5-48 h (hrs) after treatments. Following LPS administration, serum choline level increased at 0.5-24 h (P < .01), whereas serum BChE and PON1 level decreased at 48 h (P < .01) compared to their baselines. In LPS + C group, the increase in serum choline level was significantly higher (P < .01) than that of C and LPS groups. LPS did not decrease serum BChE levels significantly in calves treated with choline. Serum choline and BChE results correlated negatively with white blood cell count and positively (P < .001) with PON1 levels, oxidative stress index, inflammation and hepato-muscular injury markers. In conclusion serum choline and BChE may have a role in the pathophysiology of endotoxemia in calves. High serum choline concentration is associated with an improvement in response to LPS administration in calves treated with choline, probably by preventing the imbalances between oxidative stress and anti-oxidant capacity, preventing the serum BChE and PON1 decreases, and inhibition/attenuation of acute phase reaction and hepato-muscular injury in calves with endotoxemia.