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, 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.
Kravtsov
Gennadi M
GM
Department of Physiology, Faculty of Medicine, The University of Hong Kong, Hong Kong, ROC. gmkravts@hkucc.hk
Bruce
Iain C
IC
Wong
Tak Ming
TM
Kwan
Chiu-Yin
CY
D000199:Actins / Q000378:metabolism; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology*; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D020746:Calcium Channels, L-Type / Q000378:metabolism; D002132:Calcium Radioisotopes / Q000493:pharmacokinetics; D002413:Cations, Divalent / Q000494:pharmacology; D002614:Chelating Agents / Q000494:pharmacology; D004492:Edetic Acid / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D007552:Isotonic Solutions / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology; D008297:Male; D011108:Polymers; D011188:Potassium / Q000494:pharmacology*; D051381:Rats; D011921:Rats, Inbred WKY; D017207:Rats, Sprague-Dawley; D014661:Vasoconstriction / Q000187:drug effects* / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
D000199:Actins; D002121:Calcium Channel Blockers; D020746:Calcium Channels, L-Type; D002132:Calcium Radioisotopes; D002413:Cations, Divalent; D002614:Chelating Agents; D007552:Isotonic Solutions; D011108:Polymers; D004533:Egtazic Acid; D004492:Edetic Acid; D008274:Magnesium; D011188:Potassium; D002118:Calcium