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Carbon monoxide effects on calcium levels in vascular smooth muscle
1Department of Physiology, Texas Tech University Health Sciences Center, Lubbock 79430.
Insights
Carbon monoxide (CO) relaxes vascular smooth muscle by reducing intracellular calcium levels. This study demonstrates CO
Area of Science:
- Physiology
- Pharmacology
- Cardiovascular Research
Background:
- Carbon monoxide (CO) has been shown to relax vascular smooth muscle.
- Previous studies indicated CO-induced relaxation is independent of hypoxia, adrenergic, adenosine, or prostaglandin pathways.
Purpose of the Study:
- To investigate the effect of carbon monoxide (CO) on intracellular calcium (Ca++) concentrations in vascular smooth muscle.
- To elucidate the mechanism by which CO induces vascular relaxation.
Main Methods:
- Isolated rat thoracic aorta segments were incubated with the calcium-45 (45Ca) tracer.
- Aortic rings were exposed to oxygen (O2), nitrogen (N2), or carbon monoxide (CO) for 60 minutes.
- Verapamil was used as a positive control to validate the experimental system.
Main Results:
- Oxygen and nitrogen gas treatments resulted in Ca++ concentrations of 488 ± 35 and 515 ± 26 mM/g tissue, respectively.
- Carbon monoxide significantly reduced Ca++ concentrations by 29% to 369 ± 18 mM/g tissue (P < 0.01).
- Verapamil treatment decreased Ca++ concentrations by 40% to 314 ± 23 mM/g tissue.
Conclusions:
- Carbon monoxide (CO) decreases intracellular calcium (Ca++) concentrations in vascular smooth muscle.
- The reduction in Ca++ levels by CO is a key mechanism for its vascular smooth muscle relaxant and vasodilatory effects.
Abstract:
Previously we showed that carbon monoxide (CO) relaxes vascular smooth muscle in the working heart and thoracic aorta preparations perfused with hemoglobin-free, Krebs-Henseleit (KH) solution. The CO-induced relaxation was not caused by hypoxia, nor was it mediated by adrenergic influences, adenosine, or prostaglandins. In these studies the effect of CO on calcium (Ca++) concentrations in vascular smooth muscle was determined using 45Ca as a tracer. Isolated rat thoracic aorta segments were incubated with 45Ca and gassed with O2, N2, or CO for 60 min. Verapamil was used to verify the effectiveness of the test system. Ca++ concentrations were 488 +/- 35 and 515 +/- 26 mM/g tissue (X +/- SE) in aortic rings gassed with O2 and N2, respectively. CO reduced Ca++ concentrations significantly (P less than 0.01) by 29% to 369 +/- 18 mM/g tissue. Verapamil treatment reduced Ca++ concentrations by 40% to 314 +/- 23 mM/g tissue. These results suggest that CO relaxes vascular smooth muscle and dilates blood vessels by decreasing Ca++ concentrations in vascular smooth muscle.