Modulation of aortic smooth muscle cell membrane potential by extracellular calcium.

Palant, Carlos E.; Stern, Naftali; Meyer, Alexander; Tuck, M. L.; Lee, D. B. N.; Yanagawa, Norimoto

doi:10.1161/01.hyp.14.5.549

Cited by 8 publications

(5 citation statements)

References 29 publications

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“…These observations suggest that vascular smooth muscle intracellular activator calcium concentration on exposure to a variety of agonists is independent of the variation in extracellular Ca 2+ level used in this study. This conclusion is consistent with the observation of Palant et al 24 on rat thoracic aorta; they failed to find a change in intracellular Ca 2+ using the dye fura 2-AM when extracellular Ca 2+ was reduced to 0.25 mM. Over the same range of calcium concentration, the membrane potential of the vascular smooth muscle from the common carotid artery does not vary significantly.…”

Section: +supporting

confidence: 92%

“…Webb and Bohr 26 proposed that the reduced response of vascular strips to norepinephrine was due to increased activity of the Na + ,K + -ATPase. Furspan et al 28 introduced the idea that "membranebound calcium" reinforces the stabilizing effect of an electrical field on the resting membrane, a concept subsequently supported in part by Palant et al 24 It has been suggested that membrane stabilization is associated with Ca 2+ binding by an integral membrane Ca 2+ binding protein that presumably stabilizes a variety of membrane-related mechanisms. 28 Lopez-Jaramillo et al 18 did not advance an explanation for the reduction they observed in NO production in high extracellular Ca* + .…”

Section: +mentioning

confidence: 99%

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Calcium dependence of flow-induced dilation. Cooperative interaction with sodium.

Bevan

Joyce

1993

Hypertension

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The effect of changing extracellular calcium and sodium concentrations on flow, acetylcholine, and papaverine vasodilation and also on norepinephrine contraction was studied in a segment of a resistance branch of the rabbit central ear artery mounted in a myograph. Decreases in calcium to 80% of the normal physiological saline solution concentration (1.6 mM) reduced both flow-and acetylcholine-induced dilation. Increases of calcium to 120%, 140%, and 200% of normal decreased flow dilation responses, but not those to acetylcholine and papaverine. Thus, the optimum calcium concentration for flow dilation lies within the range of 1.4-1.9 mM. The concomitant proportionate reduction of sodium and calcium offsets the reduction in flow dilation that occurred with reduction in calcium alone. This was true whether sodium and calcium were reduced simultaneously or whether the effect of lowered sodium and then that of lowered sodium and calcium was studied. Emphasizing the uniqueness of this interaction between sodium and calcium are the observations that the depression of acetylcholine dilation by calcium reduction was not influenced by a concurrent reduction in sodium and that the depression of flow dilation caused by sodium reduction is increased by calcium increase, which by itself depresses flow dilation. None of these changes in sodium and calcium alters the responses of the artery segment to papaverine or norepinephrine. We propose that these interactions of sodium and calcium in relation to flow dilation may reflect the binding properties for sodium and calcium of a proposed flow sensor, the glycosaminoglycan polyanions. These results raise the possibility that vascular tone may be influenced not only by the absolute but by the relative concentrations of sodium and calcium. 1 -3 Intraluminal flow can also cause small artery dilation, which has been reported to be entirely 4 -6 or partly 7 endothelium dependent. In the latter case, part of the flow-induced response originates from subendothelial sites in the extracellular matrix, the smooth muscle cells, or both. Other differences and also similarities between flow-and acetylcholine-induced dilation have been reported. Flow, but not acetylcholine, dilation is sensitive to reduction in extracellular Na + concentration. 8 Both are reduced by hemoglobin and methylene blue and are potentiated by superoxide dismutase and cyclic guanosine monophosphate phosphodiesterase inhibitors.910 Acetylcholine and the endothelium-dependent component of flow dilation are prevented by substances that influence the synthesis of NO from arginine 911 ; the endothelium-independent component is not.12 Both acetylcholine and flow relaxation are reduced by amiloride.

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Section: +supporting

confidence: 92%

Section: +mentioning

confidence: 99%

Calcium dependence of flow-induced dilation. Cooperative interaction with sodium.

Bevan

Joyce

1993

Hypertension

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“…Intracellular calcium did not change when external calcium was increased from 0.25 to 1.8 mmol/L. 41 Intracellular sodium was found not to change when extracellular calcium was increased up to 1.8 mmol/L in cultured rat aortic smooth muscle cells. This was confirmed in cells cultured from the carotid artery of the same species.…”

Section: Changes In Extracellular Calciummentioning

confidence: 74%

Flow regulation of vascular tone. Its sensitivity to changes in sodium and calcium.

Bevan

1993

Hypertension

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Our hypothesis is that flow-through hydraulic drag or shear stresses the extracellular elements in the vascular wall. When the endothelium is intact, this results in the release of endothelium-derived relaxing factor and other substances, eg, prostanoids, from the endothelium. As in some reports, after inhibition of nitric oxide synthase, flow effects are still observed although diminished; the shear effect is extended mechanically to the subendothelial tissues. Shear causes conformational changes in the glycosaminoglycans by extending them from a randomly coiled aggregated state to a more elongated condition along the line of flow. This elongation and the consequent exposure of an increased number of cationic binding sites on the glycosaminoglycans lead to changes in sodium binding. The extent of the conformational change is influenced by the concentration of calcium, an ion that not only competes with sodium at specific binding sites but possibly cross-links the polysaccharide chains of the protein saccharide complex. These complex interactions might account for the cooperative, nonantagonistic interaction of sodium and calcium over the physiological concentration range. Sodium binding is influenced by changes in external sodium concentration, and this presumably accounts for the sodium sensitivity of the flow response. Although glycosaminoglycans are possibly the most studied in this regard, they are not the only candidates. Other extracellular proteins, either in conjunction with glycosaminoglycans or independently, might be involved. By mechanisms not yet identified, these changes are signaled to the cell. We have proposed that in part, at any rate, this may be related to the sodium concentration gradient.

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“…In our study the threshold concentration of [Ca"], needed to repolarize the platelets was 20 pAM. A recent study has suggested that in vascular smooth muscle cells the active level of [Ca'-]<, is in the mALI range and may affect resting En, (22). Inoue et al (24) have recently described Ca'+-activated K+ channels in portal vein cells that are opened by [Ca'+], at a threshold of 0.2-7.5 pLM; a maximal response was reached at a concentration of greater than 600 p A V .…”

Section: Discussionmentioning

confidence: 99%

Calcium-Activated Potassium Channels in Human Platelets

Fine

Hansen

Salcedo

et al. 1989

Experimental Biology and Medicine

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The cationic fluorescent probe, DiSC,(5) was used to measure the membrane potential in human platelets. Hyperpolarization was induced by the addition of Ca2+ to the medium and also by the addition of the Ca2+ ionophore, A23187. In the absence of extracellular Ca2+ ([Ca'+],) there was no response to A23187. The threshold concentration for [Ca2+]., was 20 fiM and for A23187 was 12 nM. The increase polarity induced by [Ca2+lO was not affected by various K' channel blockers. However, the effect of A23187 was inhibited by quinine and charybdotoxin, while apamin, tetraethylammonium, and the calmodulin inhibitors trifluoperarine and compound I324571 were ineffective. The resting membrane potential was -66 f 0.9 mV and was decreased by quinine. There are three conclusions from this study: (i) Ca2+-activated K+ channels exist in human platelets: (ii) they are the type that are apamin insensitive, charybdotoxin sensitive; and (iii) they may contribute to the resting membrane potential. [P.S.E.B.M. 1989[P.S.E.B.M. , VoI 1921 nimal cell plasma membranes possess K+ channels, which, when opened, induce cytoplasmic

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Modulation of aortic smooth muscle cell membrane potential by extracellular calcium.

Cited by 8 publications

References 29 publications

Calcium dependence of flow-induced dilation. Cooperative interaction with sodium.

Calcium dependence of flow-induced dilation. Cooperative interaction with sodium.

Flow regulation of vascular tone. Its sensitivity to changes in sodium and calcium.

Calcium-Activated Potassium Channels in Human Platelets

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