Summary of Endothelial [Ca2i in EDHFMediated Vasodilatation

EDHF-mediated vasodilatation appears to require the activation of endothelial IKCa and SKCa channels in order to promote smooth muscle hyperpolarization and subsequent vasodilatation. The role of endothelial [Ca2+] in this mechanism appears to be as the principal physiological activator of those channels. Therefore, factors that significantly affect the endothelial [Ca2+] response should be able to variably modulate IKCa and SKCa channel activation, and thus EDHF-mediated vasorelaxation.


1. Chen, G., Suzuki, H., and Weston, A. H. (1988). Acetylcholine releases endothelium-derived hyperpolarizing factor and EDRF from rat blood vessels. Br. J. Pharmacol. 95, 1165-1174. This article first described the nonnitric oxide, nonprostacyclin mediator of vasorelaxation as EDHF.

2. Nilius, B., and Droogmans, G. (2001). Ion channels and their functional role in vascular endothelium. Physiol. Rev. 81, 1415-1459.

3. Garland, C. J., and Plane, F. (1996). Relative importance of endothelium-derived hyperpolarizing factor for the relaxation of vascular smooth muscle in different arterial beds. In Endothelium-Derived Hyperpolarizing Factor (P. M. Vanhoutte, ed.), Vol. 1, pp. 173-179. Harwood Academic Publishers.

4. Zygmunt, P. M., and Hogestatt, E. D. (1996). Role of potassium channels in endothelium-dependent relaxation resistant to nitroarginine in the rat hepatic artery. Br. J. Pharmacol. 117, 1600-1606.

5. Chen, G. F., and Suzuki, H. (1990). Calcium dependency of the endothelium-dependent hyperpolarization in smooth muscle cells of the rabbit carotid artery. J. Physiol (Lond) 421, 521-534. This article first described the role of endothelial Ca2+ in EDHF-mediated smooth muscle hyperpolarization.

6. Nagao, T., Illiano, S., and Vanhoutte, P. M. (1992). Heterogeneous distribution of endothelium-dependent relaxations resistant to NG-nitro-l-arginine in rats. Am. J. Physiol. 263, H1090-H1094. This article is among the first to propose a higher Ca2+ threshold for EDHF-mediated responses compared with NO-mediated responses.

7. Marrelli, S. P. (2001). Mechanisms of endothelial P2Y(1)- and P2Y(2)-mediated vasodilatation involve differential [Ca2+] responses. Am. J. Physiol. Heart Circ. Physiol. 281, H1759-H1766. This article provided direct evidence for an endothelial Ca2+ threshold for initiating EDHF-mediated vasodilatation.

8. Schilling, W. P. (1989). Effect of membrane potential on cytosolic calcium of bovine aortic endothelial cells. Am. J. Physiol. 257, H778-H784.

9. Ghisdal, P., and Morel, N. (2001). Cellular target of voltage and calcium-dependent K(+) channel blockers involved in EDHF-mediated responses in rat superior mesenteric artery. Br. J. Pharmacol. 134, 1021-1028.

10. Knot, H. J., Lounsbury, K. M., Brayden, J. E., and Nelson, M. T. (1999). Gender differences in coronary artery diameter reflect changes in both endothelial Ca2+ and ecNOS activity. Am. J. Physiol. 276, H961-H969.

11. Marrelli, S. P., Eckmann, M. S., and Hunte, M. S. (2003). Role of endothelial intermediate conductance KCa channels in cerebral EDHF-mediated dilations. Am. J. Physiol Heart Circ. Physiol. 285, H1590-H1599. This article demonstrates the importance of endothe-lial Ca2+ as the physiological stimulus for endothelial hyperpolarization via activation of endothelial KCa channels.

12. Marrelli, S. P. (2002). Altered endothelial Ca2+ regulation following ischemia/reperfusion produces potentiated endothelium-derived hyperpolarizing factor-mediated dilations. Stroke 33, 2285-2291.

Capsule Biography

Dr. Marrelli is an assistant professor in the Department of Anesthesiol-ogy at Baylor College of Medicine where he studies endothelial regulation of vascular tone. In particular, Dr. Marrelli's research focuses on the blood vessels of the cerebral circulation and the effects of ischemia/reperfusion (or stroke) on subsequent vascular function.

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