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Flow-mediated dilation attenuates constriction of large coronary arteries to serotonin
1Department of Internal Medicine, University of Iowa, Iowa City 52242.
Insights
Flow-mediated dilation in coronary arteries, dependent on the endothelium, can lessen serotonin-induced constriction. This protective effect is lost when the endothelium is removed, highlighting its crucial role in regulating vascular tone.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Vascular Biology
Background:
- Coronary artery constriction can be influenced by humoral factors like serotonin.
- Endothelium-dependent vasodilation plays a role in regulating blood flow.
- The interaction between flow-mediated dilation and humorally mediated constriction is not fully understood.
Purpose of the Study:
- To test if flow-mediated endothelium-dependent dilation attenuates serotonin-induced constriction of large coronary arteries in vivo.
- To investigate the role of the endothelium in this interaction.
Main Methods:
- Measurements of large coronary artery diameter and flow in anesthetized dogs using ultrasonic dimension gauges and electromagnetic flow probes.
- Assessment of flow-mediated dilation using adenosine to increase flow.
- Evaluation of serotonin-induced constriction under conditions of increased and constant flow, with and without endothelium.
Main Results:
- Adenosine induced significant flow-mediated dilation, which was abolished by constant flow or endothelium removal.
- Serotonin caused constriction, which was significantly greater when flow was kept constant compared to when flow was allowed to increase.
- Removal of the endothelium abolished the difference in constriction between increased and constant flow conditions.
Conclusions:
- Flow-mediated dilation of large coronary arteries can attenuate serotonin-induced constriction.
- This attenuation is dependent on the presence of functional endothelium.
- Endothelial function is critical in modulating vascular responses to vasoactive substances and flow changes.
Abstract:
We tested the hypothesis that flow-mediated endothelium-dependent dilation can attenuate humorally mediated constriction of large coronary arteries in vivo. Accordingly, we measured constriction of large coronary arteries to serotonin when flow was allowed to increase and when flow was constant in the presence and absence of endothelium. The left anterior descending coronary artery of anesthetized dogs was perfused at constant pressure (100 mmHg) and diameter measured with an ultrasonic dimension gauge. Coronary flow was measured with an in-line electromagnetic flow probe. Flow-mediated dilation was demonstrated by measuring diameter (D) after increased flow in response to adenosine (1 mg/min ic). Adenosine (n = 9) increased flow (341 +/- 69%) and resulted in large artery dilation [diameter change (delta D) = 101 +/- 54 microns], which was abolished by maintaining constant flow (distal snare) or by removing endothelium. Serotonin (n = 9, 50 micrograms/min ic) increased flow (298 +/- 45%) while simultaneously decreasing large artery diameter (delta D = -58 +/- 22 microns). When flow was kept constant, serotonin produced a greater constriction (delta D = -173 +/- 29 microns). After the removal of endothelium (n = 10), constrictor responses to serotonin were similar when flow increased (delta D = -84 +/- 13 microns) and when flow was kept constant (delta D = -79 +/- 23 microns). We conclude that flow-mediated dilation of large coronary arteries can attenuate constriction to serotonin and that this effect is dependent on endothelium.