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Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up

AIM: Conduction of vasomotor responses may contribute to long‐term regulation of resistance artery function and structure. Most previous studies have addressed conduction of vasoactivity only during very brief stimulations. We developed a novel set‐up that allows the local pharmacological stimulatio...

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Autores principales: Palao, T., van Weert, A., de Leeuw, A., de Vos, J., Bakker, E. N. T. P., van Bavel, E.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6221078/
https://www.ncbi.nlm.nih.gov/pubmed/29783282
http://dx.doi.org/10.1111/apha.13099
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author Palao, T.
van Weert, A.
de Leeuw, A.
de Vos, J.
Bakker, E. N. T. P.
van Bavel, E.
author_facet Palao, T.
van Weert, A.
de Leeuw, A.
de Vos, J.
Bakker, E. N. T. P.
van Bavel, E.
author_sort Palao, T.
collection PubMed
description AIM: Conduction of vasomotor responses may contribute to long‐term regulation of resistance artery function and structure. Most previous studies have addressed conduction of vasoactivity only during very brief stimulations. We developed a novel set‐up that allows the local pharmacological stimulation of arteries in vitro for extended periods of time and studied the conduction of vasomotor responses in rat mesenteric arteries under those conditions. METHODS: The new in vitro set‐up was based on the pressure myograph. The superfusion chamber was divided halfway along the vessel into two compartments, allowing an independent superfusion of the arterial segment in each compartment. Local and remote cumulative concentration‐response curves were obtained for a range of vasoactive agents. Additional experiments were performed with the gap junction inhibitor 18β‐glycyrrhetinic acid and in absence of the endothelium. RESULTS: Phenylephrine‐induced constriction and acetylcholine‐induced dilation were conducted over a measured distance up to 2.84 mm, and this conduction was maintained for 5 minutes. Conduction of acetylcholine‐induced dilation was inhibited by 18β‐glycyrrhetinic acid, and conduction of phenylephrine‐induced constriction was abolished in absence of the endothelium. Constriction in response to high K(+) was not conducted. Absence of remote stimulation dampened the local response to phenylephrine. CONCLUSION: This study demonstrates maintained conduction of vasoactive responses to physiological agonists in rat mesenteric small arteries likely via gap junctions and endothelial cells, providing a possible mechanism for the sustained functional and structural control of arterial networks.
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spelling pubmed-62210782018-11-15 Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up Palao, T. van Weert, A. de Leeuw, A. de Vos, J. Bakker, E. N. T. P. van Bavel, E. Acta Physiol (Oxf) Cardiovascular Physiology AIM: Conduction of vasomotor responses may contribute to long‐term regulation of resistance artery function and structure. Most previous studies have addressed conduction of vasoactivity only during very brief stimulations. We developed a novel set‐up that allows the local pharmacological stimulation of arteries in vitro for extended periods of time and studied the conduction of vasomotor responses in rat mesenteric arteries under those conditions. METHODS: The new in vitro set‐up was based on the pressure myograph. The superfusion chamber was divided halfway along the vessel into two compartments, allowing an independent superfusion of the arterial segment in each compartment. Local and remote cumulative concentration‐response curves were obtained for a range of vasoactive agents. Additional experiments were performed with the gap junction inhibitor 18β‐glycyrrhetinic acid and in absence of the endothelium. RESULTS: Phenylephrine‐induced constriction and acetylcholine‐induced dilation were conducted over a measured distance up to 2.84 mm, and this conduction was maintained for 5 minutes. Conduction of acetylcholine‐induced dilation was inhibited by 18β‐glycyrrhetinic acid, and conduction of phenylephrine‐induced constriction was abolished in absence of the endothelium. Constriction in response to high K(+) was not conducted. Absence of remote stimulation dampened the local response to phenylephrine. CONCLUSION: This study demonstrates maintained conduction of vasoactive responses to physiological agonists in rat mesenteric small arteries likely via gap junctions and endothelial cells, providing a possible mechanism for the sustained functional and structural control of arterial networks. John Wiley and Sons Inc. 2018-06-17 2018-11 /pmc/articles/PMC6221078/ /pubmed/29783282 http://dx.doi.org/10.1111/apha.13099 Text en © 2018 The Authors. Acta Physiologica published by John Wiley & Sons Ltd on behalf of Scandinavian Physiological Society This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Cardiovascular Physiology
Palao, T.
van Weert, A.
de Leeuw, A.
de Vos, J.
Bakker, E. N. T. P.
van Bavel, E.
Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title_full Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title_fullStr Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title_full_unstemmed Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title_short Sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
title_sort sustained conduction of vasomotor responses in rat mesenteric arteries in a two‐compartment in vitro set‐up
topic Cardiovascular Physiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6221078/
https://www.ncbi.nlm.nih.gov/pubmed/29783282
http://dx.doi.org/10.1111/apha.13099
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