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

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 (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.

Cell-volume-dependent vascular smooth muscle contraction: role of Na+, K+, 2Cl? cotransport, intracellular Cl? and L-type Ca2+ channels

“…Thus, Kravtsov and co-workers reported that K + o -induced contractions in Mg 2+ -free medium are not mediated by Ca 2+ -influx and occur in the presence of EDTA [30]. It should be underlined, however, that in contrast to shrunken VSMR, K + o -induced contractions in Mg 2+ -free medium were suppressed by L-type channel blockers [30].…”

“…Thus, Kravtsov and co-workers reported that K + o -induced contractions in Mg 2+ -free medium are not mediated by Ca 2+ -influx and occur in the presence of EDTA [30]. It should be underlined, however, that in contrast to shrunken VSMR, K + o -induced contractions in Mg 2+ -free medium were suppressed by L-type channel blockers [30]. It was shown that Ca 2+ o -independent VSMC contractions triggered by activators of protein kinase C, tyrosine and Rhoassociated kinases were mediated by calcium sensitization of the contractile machinery [8,23,38].…”

“…Table 3 shows that 30 min preincubation with 100 μM bumetanide decreased Cl − i content by~40%, and completely abolished the rise of this parameter caused by 20 min hyperosmotic shrinkage in the presence of 150 mM sucrose. It is generally accepted that electrical excitation leads to VSMC contraction caused by Ca 2+ influx via voltagegated long-lasting (L-type) Ca 2+ channels (for references see [30]). K + o -induced depolarization of WKY-7 cells Table 2 Effect of hyper-and isosmotic shrinkage on intracellular water content and Cl − i concentration in WKY-7 cells.…”

Participation of NO in the vasodilatory action of isoespintanol

“…Contraction in vascular smooth muscle can be initiated by mechanical, electrical, and chemical stimuli. Electrical depolarization of the vascular smooth muscle cell membrane (as produced by 80 mM KCl) elicits contraction by increasing the intracellular Ca 2+ concentration, most likely by opening voltage dependent Ca 2+ channels (L-type Ca 2+ channels) (10). Accumulating evidence suggests that the transient receptor potential (TRP) channels modulate the driving force for Ca 2+ entry through L-type Ca 2+ channels and provide intracellular pathways for Ca 2+ release from cellular organelles, thus increasing the intracellular Ca 2+ concentration (11).…”