Cooling augments contractile response to 5-hydroxytryptamine via an endothelium-dependent mechanism
(1989) In Blood Vessels 26(6). p.347-359- Abstract
- The interaction between cooling and vasoactive substances, e.g. 5-hydroxytryptamine (5-HT), plays an important role in the pathophysiology of cold-induced vasospasm. Our objective was to study the effect of cooling on the 5-HT vascular response, classify the involved 5-HT receptors, and to analyze the role of the endothelium. Ring segments from the rat jugular vein, a preparation without alpha-adrenergic receptors, were suspended in organ baths to record the circular motor activity. The temperature was initially 37 degrees C and was thereafter either continuously lowered to 10 degrees C or kept constant at different temperatures within this range. 5-HT at low concentrations (10(-11) to 3 x 10(-8) M) induced relaxation at 37 degrees C in... (More)
- The interaction between cooling and vasoactive substances, e.g. 5-hydroxytryptamine (5-HT), plays an important role in the pathophysiology of cold-induced vasospasm. Our objective was to study the effect of cooling on the 5-HT vascular response, classify the involved 5-HT receptors, and to analyze the role of the endothelium. Ring segments from the rat jugular vein, a preparation without alpha-adrenergic receptors, were suspended in organ baths to record the circular motor activity. The temperature was initially 37 degrees C and was thereafter either continuously lowered to 10 degrees C or kept constant at different temperatures within this range. 5-HT at low concentrations (10(-11) to 3 x 10(-8) M) induced relaxation at 37 degrees C in segments precontracted by prostaglandin F2 alpha. The relaxation was recognized to be mediated via an endothelium-dependent 5-HT1-like receptor mechanism presumably involving the release of endothelium-derived relaxing factor (EDRF). Cooling to 29 and 20 degrees C diminished the relaxation, probably due to an attenuated release of EDRF. 5-HT at concentrations of more than 10(-8) M induced a contraction in all vessels at 37 degrees C mediated via a 5-HT2 receptor. An increased 5-HT-induced contraction was seen at temperatures below 37 degrees C in vessels with an intact endothelium. Endothelial denudation diminished the cold-induced enhancement of the contraction to 5-HT. These studies suggest that endothelial mechanisms contribute to a cold-induced augmented response to 5-HT. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1104527
- author
- Bodelsson, Mikael LU ; Arneklo-Nobin, B and Tornebrandt, K
- organization
- publishing date
- 1989
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Blood Vessels
- volume
- 26
- issue
- 6
- pages
- 347 - 359
- publisher
- Karger
- external identifiers
-
- pmid:2641924
- scopus:0024806505
- ISSN
- 0303-6847
- language
- English
- LU publication?
- yes
- id
- 1e9b888d-9d9e-4ac2-b49d-d894d0bf2015 (old id 1104527)
- date added to LUP
- 2016-04-01 16:05:40
- date last changed
- 2021-08-29 04:08:05
@article{1e9b888d-9d9e-4ac2-b49d-d894d0bf2015,
abstract = {{The interaction between cooling and vasoactive substances, e.g. 5-hydroxytryptamine (5-HT), plays an important role in the pathophysiology of cold-induced vasospasm. Our objective was to study the effect of cooling on the 5-HT vascular response, classify the involved 5-HT receptors, and to analyze the role of the endothelium. Ring segments from the rat jugular vein, a preparation without alpha-adrenergic receptors, were suspended in organ baths to record the circular motor activity. The temperature was initially 37 degrees C and was thereafter either continuously lowered to 10 degrees C or kept constant at different temperatures within this range. 5-HT at low concentrations (10(-11) to 3 x 10(-8) M) induced relaxation at 37 degrees C in segments precontracted by prostaglandin F2 alpha. The relaxation was recognized to be mediated via an endothelium-dependent 5-HT1-like receptor mechanism presumably involving the release of endothelium-derived relaxing factor (EDRF). Cooling to 29 and 20 degrees C diminished the relaxation, probably due to an attenuated release of EDRF. 5-HT at concentrations of more than 10(-8) M induced a contraction in all vessels at 37 degrees C mediated via a 5-HT2 receptor. An increased 5-HT-induced contraction was seen at temperatures below 37 degrees C in vessels with an intact endothelium. Endothelial denudation diminished the cold-induced enhancement of the contraction to 5-HT. These studies suggest that endothelial mechanisms contribute to a cold-induced augmented response to 5-HT.}},
author = {{Bodelsson, Mikael and Arneklo-Nobin, B and Tornebrandt, K}},
issn = {{0303-6847}},
language = {{eng}},
number = {{6}},
pages = {{347--359}},
publisher = {{Karger}},
series = {{Blood Vessels}},
title = {{Cooling augments contractile response to 5-hydroxytryptamine via an endothelium-dependent mechanism}},
volume = {{26}},
year = {{1989}},
}