Cytosolic calcium changes in cultured rat aortic smooth-muscle cells induced by oxyhemoglobin

✓ To clarify the mechanism of contractive effects in arteries caused by oxyhemoglobin, changes in the concentration of cytosolic calcium ([Ca++]1) before and after exposure to oxyhemoglobin were measured in vitro in cultured vascular smooth-muscle cells obtained from rat aorta. This was accomplished by preloading these cells with a fluorescent intracellular Ca++ probe fura-2/AM. Oxyhemoglobin induced a significant elevation of [Ca++]1 in vascular smooth-muscle cells which was sustained for 10 minutes. This response was completely abolished by chelating extracellular calcium with ethyleneglycol-bis (β-aminoethylether)-N,N′-tetra-acetic acid (EGTA). Oxyhemoglobin induced no accumulation of mass content of inositol 1,4,5-trisphosphate (IP3(1,4,5)). The oxyhemoglobin-induced elevation of [Ca++]1 was not blocked by verapamil, a calcium antagonist. Serotonin induced a rapid, transient increase of [Ca++]1 followed by a sustained elevation above baseline for 5 minutes. Additions of EGTA or verapamil had a small effect on the peak height of serotonin-induced [Ca++]1 elevation, but the [Ca++]1 level declined more quickly to the basal level in treated compared with control cells. These results indicate that oxyhemoglobin-induced [Ca++]1 elevation is caused by the influx of extracellular calcium, which is independent of the verapamil-blocked voltage-gated calcium channel. The long-lasting high elevation of [Ca++]1 caused by oxyhemoglobin suggests that oxyhemoglobin may contribute to the production of abnormal contractions and/or irreversible damage in vascular smooth-muscle cells.

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Hemin: levels in experimental subarachnoid hematoma and effects on dissociated vascular smooth-muscle cells

Journal of Neurosurgery ◽

10.3171/jns.1993.79.2.0252 ◽

1993 ◽

Vol 79 (2) ◽

pp. 252-255 ◽

Cited By ~ 61

Author(s):

Peter B. Letarte ◽

Kristine Lieberman ◽

Kazuhiko Nagatani ◽

Robert A. Haworth ◽

Gerard B. Odell ◽

...

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Cerebral Vasospasm ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Content Type ◽

Autologous Whole Blood ◽

The Mean ◽

Fine Print

✓ Although hemin is known to exert toxic effects on a variety of cell types, its possible participation in the genesis of cerebral vasospasm has received little attention. The authors measured the concentration of hemin in experimental subarachnoid clot and studied its effects on the morphology and 45Ca++ uptake of vascular smooth-muscle cells dissociated from canine carotid artery. Craniectomies were performed in five dogs under general anesthesia, and 3 to 5 ml of autologous whole blood was deposited in the supraclinoid subarachnoid compartment. The concentration of hemin recovered by Folch extraction from clotted material removed 7 days after surgery was 390 ± 247 µM (mean ± standard error of the mean). Mean vascular smooth-muscle cell length after 40 minutes of exposure to 50 µM hemin was 37.3 ± 1.2 µm (control 51.6 ± 1.6 µm) (p < 0.01). The mean percent permeation of 45Ca++, measured by a dual label technique, of cells exposed to hemin was 200.9% ± 23% (control 102.9% ± 4.3%) (p < 0.01). These findings indicate that hemin accrues in subarachnoid hematoma, that it exerts a constrictive effect on vascular smooth-muscle cells, and that this effect is associated with an increased uptake of Ca++. This study demonstrates that hemin should be included in the list of potential agents that participate in the development of cerebral vasospasm.

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Diadenosine Polyphosphates Increase Cytosolic Calcium and Attenuate Angiotensin-ll-lnduced Changes of Calcium in Vascular Smooth Muscle Cells

Journal of Vascular Research ◽

10.1159/000159141 ◽

1996 ◽

Vol 33 (2) ◽

pp. 132-138 ◽

Cited By ~ 9

Author(s):

Martin Tepel ◽

Jürgen Bachmann ◽

Hartmut Schlüter ◽

Walter Zidek

Keyword(s):

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Muscle Cells ◽

Cytosolic Calcium ◽

Diadenosine Polyphosphates

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Codonopsis lanceolata Contributes to Ca2+ Homeostasis by Mediating SOCE and PLC/IP3 Pathways in Vascular Endothelial and Smooth Muscle Cells

Planta Medica ◽

10.1055/a-1214-6718 ◽

2020 ◽

Vol 86 (18) ◽

pp. 1345-1352

Author(s):

Min Kyung Kim ◽

A Young Han ◽

You Kyoung Shin ◽

Kwang-Won Lee ◽

Geun Hee Seol

Keyword(s):

Endothelial Cells ◽

Smooth Muscle ◽

Vascular Smooth Muscle ◽

Smooth Muscle Cells ◽

Vascular Smooth Muscle Cells ◽

Calcium Concentration ◽

Muscle Cells ◽

Cytosolic Calcium ◽

Cytosolic Calcium Concentration ◽

Lancemaside A

Abstract Codonopsis lanceolata has been widely used as an anti-inflammatory and anti-lipogenic agent in traditional medicine. Recently, C. lanceolata was reported to prevent hypertension by improving vascular function. This study evaluated the effects of C. lanceolata and its major component lancemaside A on cytosolic calcium concentration in vascular endothelial cells and vascular smooth muscle cells. Cytosolic calcium concentration was measured using fura-2 AM fluorescence. C. lanceolata or lancemaside A increased the cytosolic calcium concentration by releasing Ca2+ from the endoplasmic reticulum and sarcoplasmic reticulum and by Ca2+ entry into endothelial cells and vascular smooth muscle cells from extracellular sources. The C. lanceolata- and lancemaside A-induced cytosolic calcium concentration increases were significantly inhibited by lanthanum, an inhibitor of non-selective cation channels, in both endothelial cells and vascular smooth muscle cells. Moreover, C. lanceolata and lancemaside A significantly inhibited store-operated Ca2+ entry under pathological extracellular Ca2+ levels. In Ca2+-free extracellular fluid, increases in the cytosolic calcium concentration induced by C. lanceolata or lancemaside A were significantly inhibited by U73122, an inhibitor of phospholipase C, and 2-APB, an inositol 1,4,5-trisphosphate receptor antagonist. In addition, dantrolene treatment, which inhibits Ca2+ release through ryanodine receptor channels, also inhibited C. lanceolata- or lancemaside A-induced increases in the cytosolic calcium concentration through the phospholipase C/inositol 1,4,5-trisphosphate pathway. These results suggest that C. lanceolata and lancemaside A increase the cytosolic calcium concentration through the non-selective cation channels and phospholipase C/inositol 1,4,5-trisphosphate pathways under physiological conditions and inhibit store-operated Ca2+ entry under pathological conditions in endothelial cells and vascular smooth muscle cells. C. lanceolata or lancemaside A can protect endothelial cells and vascular smooth muscle cells by maintaining cytosolic calcium concentration homeostasis, suggesting possible applications for these materials in diets for preventing vascular damage.

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