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Altered vascular reactivity induced by malaria parasites
C R Nwokocha1, I O Ajayi, A B Ebeigbe
1Section of Physiology, Department of Basic Medical Sciences, The University of the West Indies, Kingston 7, Jamaica, West Indies. chukwuemeka.nwokocha@uwimona.edu.jm
Objective:
In this study, we have examined the possibility that there is altered vascular reactivity due to the direct interaction between parasitized erythrocytes and vascular endothelial cells.
Method:
Ring preparations of rat aorta were studied using standard in vitro techniques, the rings were mounted in 20 ml organ baths containing PSS under an initial load of 1 g, maintained at 37 degrees C at pH 7.4 and isometric contractions were recorded electronically. Rings were allowed 90 minutes to equilibrate before the commencement of the various protocols: Dose responses to phenylephrine (PE) and other vasoactive agents (high-K+). Acetylcholine (Ach)--induced relaxation in phenylephrine-contracted rings (pre-contraction was induced by EC70 concentration of phenylephrine). Ach-induced relaxation in PE-precontracted, endothelium-denuded rings. Also, relaxation responses to acetylcholine was investigated through application of a single. (EC70) concentration of acetylcholine in rings exposed to blood with varying concentrations and dilutions of parasitized blood and varying durations of exposure.
Results:
Incubation with parasitized blood resulted in a significant increase in maximum contractile response to phenylephrine in the rat aortic rings (p < 0.05) but no effect to the base line. Analysis of the whole dose-response curve (using paired t-test) showed a significant left-ward shift following the addition of parasitized blood (p < 0.05), EC70 (M) values increasing from 7 x 10(-7) to 5 x 10(-6)M. Following exposure to parasitized blood, the magnitude of Ach-induced relaxation responses reduced significantly from 73 +/- 3.6 to 24.75 +/- 7.25% in rat aortic rings (p < 0.05). Ach relaxations were significantly enhanced (p < 0.05) at 5-minute exposure; however at longer durations, Ach-relaxations were variable and inconsistent. The lesser the dilution, due to increased volume of parasitized blood, the lesser the relaxation response. Following endothelium removal, there was a marked impairment in endothelium-dependent relaxation responses to ACh in both the control and incubated vessels. Exposure to parasitized blood did not significantly alter contractile responses induced by potassium depolarization.
Conclusions:
This gives evidence in support of an endothelium-dependent action of malaria parasites as vascular effects of malaria parasites are mediated, at least in part, via endothelium-dependent mechanism(s).
Insights
Malaria parasites alter rat aortic ring reactivity by impairing endothelium-dependent relaxation. This suggests malaria
Area of Science:
- Vascular biology
- Parasitology
- Cardiovascular research
Background:
- Malaria infection can lead to significant vascular complications.
- The direct impact of parasitized erythrocytes on vascular endothelial cells is not fully understood.
- Understanding these interactions is crucial for managing malaria-associated pathologies.
Purpose of the Study:
- To investigate the potential for altered vascular reactivity due to direct interaction between parasitized erythrocytes and vascular endothelial cells.
- To elucidate the role of the endothelium in malaria-induced vascular dysfunction.
Main Methods:
- In vitro study using isolated rat aortic ring preparations.
- Assessment of contractile responses to phenylephrine and high-potassium solutions.
- Evaluation of acetylcholine-induced relaxation in intact and endothelium-denuded rings, with and without exposure to parasitized blood.
Main Results:
- Exposure to parasitized blood significantly increased contractile responses to phenylephrine.
- Parasitized blood significantly reduced acetylcholine-induced relaxation, indicating impaired endothelial function.
- These effects were dependent on the concentration of parasitized blood and duration of exposure.
Conclusions:
- Malaria parasites exert endothelium-dependent effects on vascular reactivity.
- Vascular dysfunction in malaria is, at least partly, mediated by mechanisms involving the vascular endothelium.
- These findings highlight the endothelium as a key target in malaria-related vascular complications.
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