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A new view of K+-induced contraction in rat aorta: the role of Ca2+ binding

  • Cardiovascular System
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Abstract

Strong, K+-induced contractions of rat aorta in Ca-free, Mg-free media were not accompanied by increased intracellular calcium concentration, [Ca2+]i, whereas such contractions in the presence of the divalent cations were correlated with rising [Ca2+]i as assessed by fura-2. At the same time, calcium channel blockers, a modulator of Ca2+-binding proteins, and a modulator of actin polymerization, inhibited all types of K+-induced contractions. Increasing the K+ in isotonic medium evoked a rise of 45Ca2+ binding to the plasma membrane of freshly isolated aortic cells. Although Ca2+-dependent events underlie the mechanism of K+-induced vascular contractions in both the presence and absence of Ca2+, in contrast to the view that [Ca2+]i is a key regulator of excitation-contraction coupling in smooth muscle, we suggest that the modulation of Mg2+-dependent Ca2+ binding, probably within/at the L-type calcium channel by K+, is a trigger for aortic contraction. This Ca2+ binding may then activate actin-myosin interaction.

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Acknowledgements

We thank Dr. F. Mo (The University of Hong Kong) for help in developing the fluorescent method for evaluation of [Ca2+]i in the rat aorta.

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Correspondence to Gennadi M. Kravtsov.

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Kravtsov, G.M., Bruce, I.C., Wong, T.M. et al. A new view of K+-induced contraction in rat aorta: the role of Ca2+ binding. Pflugers Arch - Eur J Physiol 446, 529–540 (2003). https://doi.org/10.1007/s00424-003-1096-x

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  • DOI: https://doi.org/10.1007/s00424-003-1096-x

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