Publication Database

Evidence for the stimulation of multiple conductances by cinnemaldehyde in the porcine colon (2018)

Art

Poster

Autoren

Manneck, D (WE 2)

Schrapers, KT (WE 2)

Stumpff, F (WE 2)

Kongress

23. Tagung der DVG-Fachgruppe Physiologie und Biochemie der Deutschen Veterinärmedizinischen Gesellschaft

Wien, 21. – 23.02.2018

Quelle

23. Tagung der Fachgruppe Physiologie und Biochemie der Deutschen Veterinärmedizinischen Gesellschaft : PROGRAMM & ABSTRACTS — Veterinärmedizinische Universität Wien (Hrsg.)

Wien, 2018 — S. 64

ISBN: 978-3-86345-307-7

Sprache

Englisch

Verweise

URL (Volltext): https://www.vetmeduni.ac.at/fileadmin/v/DVG-Tagung-2018/160218_Abstract_Program_Guide_sortiert_final.pdf

Kontakt

Institut für Veterinär-Physiologie

Oertzenweg 19 b
14163 Berlin
+49 30 838 62600
physiologie@vetmed.fu-berlin.de

Abstract / Zusammenfassung

Phytonutrients are being investigated for their potential to improve the efficiency of nutrient digestion, but effects on ion transport have rarely been discussed. Colon of pigs was mounted in Ussing chambers at 37°C and gassed with carbogen. Changes in short circuit current (Isc) and tissue conductance (Gt) were used to monitor effects of adding 1 mmol·l-1 cinnamaldehyde after replacement of an ion or addition of a blocker. For data evaluation, the changes in Isc and Gt were calculated 15 minutes after the ion replacement or blocker and 15 minutes after addition of cinnamaldehyde. In standard NaCl buffer solution, mean Isc was 9.10 ± 2.12 μA·cm-2 and mean Gt 20.34 ± 0.75 mS·cm-2. Addition of 1 mmol·l-1 cinnamaldehyde led to significant increases of Isc and Gt by ΔIcinn = 18.35 ± 2.15 μA·cm-2 and ΔGcinn = 4.72 ± 0.35 mS·cm-2 (both p < 0.001). To test for neuronal involvement, 1 mmol·l-1 lidocaine was applied, which showed no effect on either ΔIcinn or ΔGcinn (p > 0.7). Chloride secretion was inhibited by low chloride solution (9.8 mmol·l-1, both sides), 0.5 mmol·l-1 NPPB, 1 mmol·l-1 bumetanide, or 0.01 mmol·l-1 indometacin. Low chloride or bumetanide had no significant effect on ΔIcinn (p > 0.1), while effects of indometacin and NPPB were only partial (62% and 47%, p < 0.001). Of these interventions, only low chloride had a small effect on ΔGcinn, which was reduced by 25% (p = 0.037). Conversely, bilateral replacement of Na+ by NMDG+ significantly reduced both ΔIcinn and ΔGcinn (by 86% and 79%, both p < 0.001), probably reflecting both effects on Na+ transport and inhibition of basolateral NKCC. Replacement of mucosal Na+ reduced ΔGcinn (p < 0.001), while ΔIcinn remained unchanged. The ENaC blocker amiloride (1 mmol·l-1) showed no effect on the cinnamaldehyde response. Conversely, 1 mmol·l-1 quinidine significantly reduced ΔGcinn (p < 0.001). Replacement of mucosal Ca2+ by 1 mmol·l-1 EGTA increased ΔGcinn (p < 0.002). Numerically, ΔIcinn dropped in response to quinidine and rose in response to EGTA, most likely reflecting simultaneous changes of Na+ absorption and K+ secretion through the pore of a non-selective cation channel.

The data suggest that roughly half of the cinnamaldehyde response is related to cAMP dependent chloride secretion, most likely via NKCC and CFTR. Quinidine sensitive, amiloride insensitive cation channels may represent the other half of the conductance.