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Updated: Aug 18, 2026
Intracoronary Acetylcholine Provocation Testing for Assessment of Coronary Vasomotor Disorders
Published on: August 18, 2016
Coronary vasoconstriction by locally administered acetylcholine, carbachol and bethanechol in isolated,
Insights
Acetylcholine, carbachol, and bethanechol cause coronary vasoconstriction in rats by activating muscarinic receptors. These findings are crucial for understanding cardiovascular drug actions and developing new treatments.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
Background:
- The coronary vasculature plays a critical role in regulating myocardial blood flow.
- Understanding the specific receptors involved in coronary vascular tone is essential for cardiovascular drug development.
Purpose of the Study:
- To investigate the role of muscarinic receptors in mediating the coronary vascular effects of acetylcholine, carbachol, and bethanechol in isolated rat hearts.
Main Methods:
- Isolated rat heart preparations were perfused at a constant flow rate.
- Drugs were injected into the aortic cannula, and perfusion pressure (PP), left ventricular pressure (LVP), and heart rate (HR) were monitored.
- Experiments included pretreatment with reserpine, phentolamine, hexamethonium, and atropine.
Main Results:
- Acetylcholine, carbachol, and bethanechol induced dose-dependent coronary vasoconstriction (increased PP).
- These effects were abolished when coronary vessels were excluded from perfusion.
- Atropine significantly antagonized the vasoconstrictor response, while reserpine, phentolamine, and hexamethonium did not.
Conclusions:
- The coronary vasoconstrictor actions of acetylcholine, carbachol, and bethanechol in the rat are mediated by muscarinic receptors.
- These findings highlight the importance of muscarinic receptor signaling in regulating coronary blood flow.
Abstract:
1 Experiments were carried out on rat isolated heart preparations in which the coronary vasculature was perfused through the aorta at a constant flow rate with arterial blood from donor animals. Single doses of drugs were injected into the aortic cannula. 2 Small doses of acetylcholine, carbachol or bethanechol decreased perfusion pressure (PP) without markedly affecting left ventricular pressure (LVP) and heart rate (HR); larger doses of these drugs increased PP (vasoconstriction), and decreased LVP and HR in a dose-dependent manner. 3 Acetylcholine, carbachol and bethanechol had almost no effects when perfused through the aorta in such a way as to exclude the coronary vessels. 4 Coronary vasoconstriction in response to acetylcholine, carbachol and bethanechol was not significantly affected by reserpine pretreatment, phentolamine or hexamethonium, but was antagonized by small doses of atropine. 5 From these results it is concluded that in the coronary vasculature of the rat, the receptors involved in the vasoconstrictor actions of acetylcholine carbachol and bethanechol are muscarinic.
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