Erythropoietin increases cytosolic free calcium concentration in vascular smooth muscle cells

1993 ◽  
Vol 27 (7) ◽  
pp. 1233-1236 ◽  
Author(s):  
M. Neusser ◽  
M. Tepel ◽  
W. Zidek
2001 ◽  
Vol 281 (3) ◽  
pp. H1156-H1162 ◽  
Author(s):  
Stéphane Budel ◽  
Alexander Schuster ◽  
Nikos Stergiopoulos ◽  
Jean-Jacques Meister ◽  
Jean-Louis Bény

We tested the hypothesis that the cytosolic free calcium concentration in endothelial cells is under the influence of the smooth muscle cells in the coronary circulation. In the left descending branch of porcine coronary arteries, cytosolic free calcium concentration ([Ca2+]i) was estimated by determining the fluorescence ratio of two calcium probes, fluo 4 and fura red, in smooth muscle and endothelial cells using confocal microscopy. Acetylcholine and potassium, which act directly on smooth muscle cells to increase [Ca2+]i, were found to indirectly elevate [Ca2+]i in endothelial cells; in primary cultures of endothelial cells, neither stimulus affected [Ca2+]i, yet substance P increased the fluorescence ratio twofold. In response to acetylcholine and potassium, isometric tension developed by arterial strips with intact endothelium was attenuated by up to 22% ( P < 0.05) compared with strips without endothelium. These findings suggest that stimuli that increase smooth muscle [Ca2+]i can indirectly influence endothelial cell function in porcine coronary arteries. Such a pathway for negative feedback can moderate vasoconstriction and diminish the potential for vasospasm in the coronary circulation.


1987 ◽  
Vol 248 (3) ◽  
pp. 883-887 ◽  
Author(s):  
J Pfeilschifter ◽  
U T Rüegg

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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