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

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, c...

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Bibliographic Details
Published in:Pflügers Archiv 2003-08, Vol.446 (5), p.529-540
Main Authors: Kravtsov, Gennadi M, Bruce, Iain C, Wong, Tak Ming, Kwan, Chiu-Yin
Format: Article
Language:English
Subjects:
Actins - metabolism
Animals
Aorta, Thoracic - physiology
Calcium
Calcium - metabolism
Calcium Channel Blockers - pharmacology
Calcium Channels, L-Type - metabolism
Calcium Radioisotopes - pharmacokinetics
Cations, Divalent - pharmacology
Chelating Agents - pharmacology
Edetic Acid - pharmacology
Egtazic Acid - pharmacology
Isotonic Solutions - pharmacology
Magnesium - pharmacology
Male
Polymers
Potassium - pharmacology
Rats
Rats, Inbred WKY
Rats, Sprague-Dawley
Vasoconstriction - drug effects
Vasoconstriction - physiology
Vasodilation - drug effects
Vasodilation - physiology
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Summary: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 (45)Ca2+ 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.
ISSN:0031-6768
1432-2013
DOI:10.1007/s00424-003-1096-x