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Vascular contractions to serotonin are augmented by cooling
C T Harker1, L M Taylor, J M Porter
1Department of Surgery, Oregon Health Sciences University, Portland 97201.
Journal of Cardiovascular Pharmacology
|December 11, 1991
Summary
Acute moderate cooling enhances serotonin-induced contractions in human saphenous veins and rat tail arteries. This temperature-dependent increase in serotonin (5-HT) receptor activity may contribute to cold-induced vasospasm.
Area of Science:
- Vascular pharmacology
- Cardiovascular research
- Physiology
Background:
- Serotonin (5-HT) is a key mediator of vascular tone.
- Cold exposure can trigger vasospasm, but underlying mechanisms are not fully understood.
- The role of temperature in modulating 5-HT-induced vascular responses requires further investigation.
Purpose of the Study:
- To investigate the effect of acute moderate cooling on vascular reactivity in human saphenous veins (HSV) and rat tail arteries (RTA).
- To determine if temperature influences serotonin (5-HT)-mediated contractions via S2 receptors.
- To explore the potential clinical implications for cold-induced vasospasm.
Main Methods:
- Isometric tension recordings were performed on isolated rings of HSV and RTA.
- Vascular responses to potassium chloride (KCl) and serotonin (5-HT) were measured at different temperatures (37°C and 24°C).
- The effects of alpha-adrenoceptor blockade and S2-selective 5-HT antagonist (ketanserin) were assessed.
Main Results:
- Cooling did not significantly affect resting tension or KCl-induced contractions.
- Serotonin (5-HT) elicited concentration-dependent contractions in both HSV and RTA, mediated by S2 receptors.
- Acute moderate cooling significantly augmented 5-HT-induced contractions in both vascular preparations.
Conclusions:
- Acute moderate cooling potentiates S2-receptor-mediated vascular contractions induced by serotonin.
- Temperature-dependent enhancement of serotonergic responsiveness may contribute to vasospasm in cold conditions.
- Findings highlight a potential mechanism linking environmental temperature to cardiovascular events.