Related Experiment Video
Updated: Jul 18, 2026
10:20
In vitro Measurements of Tracheal Constriction Using Mice
Published on: June 25, 2012
Acrolein generation stimulates hypercontraction in isolated human blood vessels
D J Conklin1, A Bhatnagar, H R Cowley
1Institute of Molecular Cardiology, Department of Medicine, University of Louisville, Louisville, KY 40202, USA. dj.conklin@louisville.edu
Toxicology and Applied Pharmacology
|November 11, 2006
Summary
Acrolein, a compound linked to oxidative stress, causes dangerous blood vessel constriction (vasospasm) in humans. This effect is amplified in hypertension and mediated by semicarbazide-sensitive amine oxidase activity.
Area of Science:
- Biomedical Science
- Cardiovascular Research
- Toxicology
Background:
- Vasospasm is linked to atherosclerosis, smoking, and hypertension, conditions involving oxidative stress and inflammation.
- Acrolein, an aldehyde derived from lipid peroxidation and inflammation, is implicated in vasospasm.
Purpose of the Study:
- To investigate the role of acrolein in human vasospasm using an ex vivo model.
- To determine the mechanism of acrolein-induced vasospasm, focusing on semicarbazide-sensitive amine oxidase (SSAO) activity and calcium ion dependency.
Main Methods:
- Utilized human coronary artery bypass graft (CABG) blood vessels for ex vivo studies.
- Exposed vessels to acrolein, allylamine (an acrolein precursor), and hydrogen peroxide, assessing responses and sensitivity.
- Investigated the role of SSAO by using SSAO inhibitors and tested other SSAO substrates and extracellular calcium's contribution.
Main Results:
- Acrolein and allylamine, but not H(2)O(2) or other tested amines, induced intractable hypercontraction in human CABG vessels.
- Allylamine-induced hypercontraction and SSAO activity were inhibited by SSAO inhibitors (semicarbazide, MDL 72274-E) but not the inactive isomer (MDL 72274-Z).
- Hypercontraction was attenuated in a calcium-free environment and enhanced in hypertensive rat aortas.
Conclusions:
- Acrolein generation in blood vessel walls increases susceptibility to vasospasm.
- SSAO activity and extracellular calcium are critical in acrolein-mediated vasospasm.
- Hypertension exacerbates acrolein-induced vasospasm.
More Related Videos
Related Concept Videos
01:17Autoregulation of Blood Flow
Autoregulation mechanisms are characterized by their inherent capacity for self-regulation without necessitating specific nervous stimulation or endocrine control. These mechanisms facilitate the adjustment of blood flow and, therefore, perfusion specific to each tissue region. This self-regulation encompasses chemical signals and myogenic controls.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.
Chemical Signaling in Autoregulation
Chemical signaling operates at the precapillary sphincter level, inciting either contraction or relaxation.
01:25Smooth Muscle Contraction
Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
The onset of contraction is triggered by an increase in calcium ions within the sarcoplasm, similar to the process in striated muscle. However, smooth muscles have a relatively smaller reservoir of the sarcoplasmic...
01:16Vascular Spasm
The vascular phase, also known as vasospasm, is the initial stage of hemostasis, crucial for preventing excessive bleeding when a blood vessel is injured. After a vessel is cut, nerves in the damaged area trigger pain and other sensory impulses. Simultaneously, the smooth muscles in the vessel wall contract, resulting in a vascular spasm. This contraction reduces the vessel's diameter at the injury site, slowing or stopping blood loss through the vessel wall. Vascular spasms typically last for...
01:28Nitric Oxide Signaling Pathway
Nitric oxide (NO), an inorganic gas, acts as a potent second messenger in most animal and plant tissues. NO diffuses out of the cells that produce it and enters the neighboring cells to generate a downstream response. NO synthase (NOS) catalyzes NO production by the deamination of the amino acid arginine. There are three isoforms of NOS. Endothelial cells have endothelial NOS (eNOS), nerve and muscle cells have neuronal NOS (nNOS), and macrophages produce inducible NOS (iNOS) upon exposure to...
00:59Direct-Acting Cholinergic Agonists: Pharmacological Actions
Direct-acting cholinergic agonists exert their pharmacological actions by mimicking the effects of acetylcholine on postsynaptic muscarinic receptors to generate parasympathetic responses. These agents elicit a range of physiological responses, including cardiovascular effects. For example, activation of muscarinic receptors induces bradycardia, decreased cardiac output, reduced peripheral resistance, and consequent hypotension. In the eye, stimulation of M3 receptors leads to smooth muscle...
01:15Muscle Contraction