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YEGEN, BERRAK

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YEGEN

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BERRAK

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Now showing 1 - 5 of 5
  • Publication
    Inhibitory effects of gastrin releasing peptide on gastric emptying in rats
    (ELSEVIER SCIENCE BV, 1996) YEGEN, BERRAK; Yegen, BC; Gurbuz, V; Coskun, T; Bozkurt, A; Kurtel, H; Alican, I; Dockray, GJ
    Gastrin-releasing peptide (GRP) has a wide range of biological actions, including stimulation of the frequency of antral contractions and delaying gastric emptying. The present study was designed to evaluate the role of GRP in the control of gastric emptying of liquid test meals in the rat. The emptying of methyl cellulose given by gavage to fasted rats, or of saline given via the fistula to conscious gastric fistula rats was not influenced by the GRP antagonists, NC-8-89 (Leu(13)-psi-(CH2NH)-Leu(14)-bombesin) and 2258U89 ((de-NH2)Phe(19),D-Ala(24),D-Pro(26)psi (CH2NH)Phe(27)(-GRP (19-27)), at 2 mg/kg, s.c. However, both antagonists (0.02, 0.2 and 2 mg/kg) reversed the inhibitory effect of HCl on gastric emptying in gastric fistula rats (P < 0.05-0.001). When peptone was administered after a preload, but not otherwise, the inhibition of emptying was also partly reversed by both antagonists at all doses used (P < 0.05-0.001). Interestingly, the delay in the emptying of hyperosmolal saline compared to saline, was enhanced at a dose of 0.2 mg/kg of both antagonists (P < 0.05 and P < 0.01). Food intake did not change significantly with the two lower doses of antagonists, but was decreased by the highest dose of NC 8-89. We conclude that GRP specifically inhibits gastric emptying of acid and peptone solutions in the conscious rat.
  • Publication
    THE HYPOTENSIVE EFFECT OF CISAPRIDE IN RAT
    (ELSEVIER SCIENCE INC, 1994) YEGEN, BERRAK; ONAT, F; YEGEN, B; BERKMAN, K; OKTAY, S
    1. Cisapride is a prokinetic agent believed to facilitate acetylcholine release from the myenteric plexus of the gut. The aim of the present study was to investigate the effect of cisapride on blood pressure and the effects of muscarinic receptor antagonists on the cisapride-induced blood pressure changes. 2. Cisapride was given i.v. alone or 10 min after muscarinic receptor antagonists. Cisapride given i.v. produced a significant decrease in blood pressure in a dose-related manner. Atropine, AF-DX 116 and 4-DAMP given 10 min before cisapride injection, partially inhibited the hypotensive response to cisapride. In pithed rat, the effect of cisapride on blood pressure remained unaltered. 3. This study indicates that the action of cisapride is not through central mechanisms and part of cisapride's effect is through the cholinergic system.
  • Publication
    CARDIOVASCULAR EFFECTS OF CENTRALLY ACTIVE CHOLINOMIMETICS IN CONSCIOUS AND ANESTHETIZED RATS - THE ROLE OF AMYGDALA
    (PERGAMON-ELSEVIER SCIENCE LTD, 1995) YEGEN, BERRAK; OZKUTLU, U; COSKUN, T; ONAT, F; YEGEN, BC; OKTAY, S
    Central cardiovascular effects of cholinergic agonists depend on the dose, site and mode of administration, species, and to the state of the animal. Intravenous injection of physostigmine and intracerebroventricular injection of carbachol produced presser and tachycardic responses in urethane-anesthetized rats. Both agents also elicited presser responses in conscious rats, but bradycardia occurred in the presence of anesthesia, Additionally, presser responses to physostigmine, but not to carbachol, were significantly exaggerated by urethane anesthesia. These results demonstrate that anesthesia depresses cardiovascular reflexes and the inhibitory control mechanisms on acetylcholine release from the nerve endings involved in cardiovascular regulation. The role of the central nucleus of the amygdala (CNA) was also investigated in this study. The presser effects of intracerebroventricular injection of carbachol were significantly attenuated by electrolytic ablation of the CNA, but heart rate changes were not altered both in anesthetized and conscious rats. These results indicate that the CNA plays a role in cholinergic control of blood pressure, but not in the regulation of heart rate.
  • Publication
    The effect of nitric oxide synthase blockade and indometacin on gastric emptying and gastric contractility
    (KARGER, 1997) YEGEN, BERRAK; Corak, A; Coskun, T; Alican, I; Kurtel, H; Yegen, BC
    The aim of the present study was to investigate the effect of nitric oxide (NO) synthase inhibition on gastric emptying rate in conscious rats and on gastric muscle contractility. The involvement of NO was also investigated in indometacin-induced (25 mg/kg, s.c.) changes in gastric emptying rate and smooth muscle contractility. L-NAME (N-G-nitro-L-arginine methyl ester; 10 mg/kg, i.v.) inhibited the gastric emptying rate compared to controls and this effect was abolished by L-arginine (300 mg/kg, i.v.). Similarly, indometacin treatment led to a significant delay of gastric emptying rate with respect to vehicle-treated rats. Gastric longitudinal and circular muscle strips of L-NAME or indometacin-treated rats showed a reduction in contractile responses to carbachol. The results demonstrate that NO synthase blockade and indometacin treatment delay gastric emptying in conscious rats, concomitant with reduced responsiveness to carbachol, in vitro.
  • Publication
    INFLUENCE OF PIRENZEPINE ON GALLBLADDER CONTRACTION IN MAN INDUCED BY SHAM FEEDING OR AN INTRADUODENAL MEAL
    (KARGER, 1992) YEGEN, BERRAK; TANKURT, E; YEGEN, BC; BIREN, T; GURMEN, N; ONAT, F; ERCIL, A; OKTAY, S; ULUSOY, NB
    Pirenzepine, an M1 muscarinic receptor antagonist, was tested for its ability to antagonize sham feeding- and intraduodenal fatty meal-stimulated gallbladder contraction in man. Intravenously administered pirenzepine abolished sham feeding-induced gallbladder contraction. Pirenzepine also inhibited contraction induced by intraduodenal meal, but this inhibition was of a lesser magnitude than the inhibition of sham feeding-induced contraction. The results demonstrate that the cephalic phase of gallbladder contraction is probably mediated by M1 muscarinic receptors while the duodenal phase of gallbladder contraction is partially mediated by M1 receptors.