Related Experiment Video
Updated: Mar 26, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Propofol-induced Inhibition of Catecholamine Release Is Reversed by Maintaining Calcium Influx
Liping Han1, Stephen Fuqua, Quanlin Li
1From the Department of Anesthesiology (L.H., X.H.) and Department of Thoracic Surgery, Dalian Municipal Friendship Hospital (L.Z.), Dalian Medical University, Dalian, Liaoning, China; Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, Virginia (S.F., G.L.); Department of Urology, the First Affiliated Hospital (Q.L.) and Department of Physiology (A.L.), Dalian Medical University, Dalian, Liaoning, China; Division of Fundamental Neurobiology, Toronto Western Research Institute, University Health Network, Toronto, Ontario, Canada (L.H., S.G., R.S., S.S.); and Department of Physiology, University of Toronto, Toronto, Ontario, Canada (S.S.).
Background:
Propofol (2,6-diisopropylphenol) is one of the most frequently used anesthetic agents. One of the main side effects of propofol is to reduce blood pressure, which is thought to occur by inhibiting the release of catecholamines from sympathetic neurons. Here, the authors hypothesized that propofol-induced hypotension is not simply the result of suppression of the release mechanisms for catecholamines.
Methods:
The authors simultaneously compared the effects of propofol on the release of norepinephrine triggered by high K-induced depolarization, as well as ionomycin, by using neuroendocrine PC12 cells and synaptosomes. Ionomycin, a Ca ionophore, directly induces Ca influx, thus bypassing the effect of ion channel modulation by propofol.
Results:
Propofol decreased depolarization (high K)-triggered norepinephrine release, whereas it increased ionomycin-triggered release from both PC12 cells and synaptosomes. The propofol (30 μM)-induced increase in norepinephrine release triggered by ionomycin was dependent on both the presence and the concentration of extracellular Ca (0.3 to 10 mM; n = 6). The enhancement of norepinephrine release by propofol was observed in all tested concentrations of ionomycin (0.1 to 5 μM; n = 6).
Conclusions:
Propofol at clinically relevant concentrations promotes the catecholamine release as long as Ca influx is supported. This unexpected finding will allow for a better understanding in preventing propofol-induced hypotension.
More Related Videos
Related Concept Videos
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Drugs Affecting Neurotransmitter Release or Uptake
Depolarizing Blockers: Mechanism of Action
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because...
Feedback Regulation of Calcium Concentration
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...
Adrenergic Agonists: Indirect-Acting Agents
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
Antihypertensive Drugs: Action of Calcium Channel Blockers

