scholarly journals Cytosolic Free Calcium Elevation in Vascular Smooth Muscle Cells Induced by Cerebrospinal Fluid from Patients with Subarachnoid Hemorrhage

1995 ◽  
Vol 35 (1) ◽  
pp. 8-12 ◽  
Author(s):  
Toshihiko NAKASHIMA ◽  
Katsunobu TAKENAKA ◽  
Seiji FUKAZAWA ◽  
Koh YANO ◽  
Yasuaki NISHIMURA ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Smooth Muscle ◽  
Subarachnoid Hemorrhage ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Elevation

Induction of cytosolic free calcium elevation in rat vascular smooth-muscle cells by cerebrospinal fluid from patients after subarachnoid hemorrhage

1991 ◽  
Vol 75 (3) ◽  
pp. 452-457 ◽  
Author(s):  
Katsunobu Takenaka ◽  
Hiromu Yamada ◽  
Noboru Sakai ◽  
Takashi Ando ◽  
Toshihiko Nakashima ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Elevation

✓ The purpose of this study was to determine the effects of cerebrospinal fluid (CSF) from patients with subarachnoid hemorrhage (SAH) on cytosolic free calcium in cultured rat vascular smooth-muscle cells using the fluorescent intracellular calcium indicator fura-2/AM. Samples of CSF were collected from 12 patients (seven with and five without vasospasm) on Days 2, 6, 11, and 16 after SAH. Control CSF samples were obtained from five patients 6 to 9 months after they had undergone successful aneurysm surgery following an SAH. All CSF samples in both the non-vasospasm and vasospasm groups, regardless of the day of sampling after the SAH, induced significantly higher transient intracellular calcium elevations when compared to levels induced by control CSF. Furthermore, the addition of 2 mM ethyleneglycol-bis (β-aminoethylether)-N,N'-tetra-acetic acid (EGTA) caused a slight reduction in the peak height in the CSF-induced intracellular calcium rise which declined more rapidly to basal levels than those studied without EGTA. In the non-vasospasm group, the intracellular calcium concentration remained stable after SAH throughout the study period. In contrast, in the vasospasm group, this concentration was highest on Day 2 post-SAH, but sharply decreased on Day 6 and rose again on Day 11. This result correlated with the clinical signs of vasospasm in these patients. These findings indicated that the intracellular calcium elevations induced by CSF obtained after SAH were due to the combination of the influx of extracellular calcium and the mobilization of intracellular calcium from storage sites. The changes in intracellular calcium concentrations in vascular smooth-muscle cells induced by CSF obtained from patients on successive days following SAH suggest that the substances that induce this repeat calcium elevation on Day 11 post-SAH may be the key spasmogens for vasospasm after SAH.

Purification of a factor from CSF in patient after SAH which induces the cytosolic free calcium elevation in vascular smooth muscle cells

1997 ◽  
Vol 19 (1) ◽  
pp. 51-56 ◽  
Author(s):  
Toshihiko Nakashima ◽  
Katsunobu Takenaka ◽  
Seiji Fukazawa ◽  
Akashi Ando ◽  
Noboru Sakai ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Calcium Elevation

scholarly journals Cyclosporin A augments angiotensin II-stimulated rise in intracellular free calcium in vascular smooth muscle cells

1987 ◽  
Vol 248 (3) ◽  
pp. 883-887 ◽  
Author(s):  
J Pfeilschifter ◽  
U T Rüegg
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Cyclosporin A ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Immunosuppressive Drug ◽  
Free Calcium ◽  
Cytosolic Free Calcium

Pretreatment of rat vascular smooth muscle cells with the immunosuppressive drug cyclosporin A caused concentration- and time-dependent increases in both the amplitude and duration of the angiotensin II-induced rise in cytosolic free calcium, as measured with quin 2. Cyclosporin A had no significant effect on basal quin 2 fluorescence. However, cyclosporin A increased the basal 45Ca2+ influx. This stimulation of 45Ca2+ influx was not blocked by nifedipine (10(-6) M). Cyclosporin A also augmented the angiotensin II-stimulated influx and efflux of 45Ca2+. These results demonstrate that cyclosporin A increases the permeability of the plasma membrane for Ca2+ and also augments the angiotensin II-induced increases in cytosolic free calcium.

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