scholarly journals Cytosolic free calcium levels in monolayers of cultured rat aortic smooth muscle cells. Effects of angiotensin II and vasopressin.

1985 ◽  
Vol 260 (13) ◽  
pp. 7836-7842 ◽  
Author(s):  
A M Capponi ◽  
P D Lew ◽  
M B Vallotton
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Free Calcium ◽  
Cytosolic Free Calcium ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

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.

Mechanism of angiotensin II-induced arachidonic acid metabolite release in aortic smooth muscle cells: involvement of phospholipase D

1997 ◽  
Vol 136 (2) ◽  
pp. 207-212 ◽  
Author(s):  
Junji Shinoda ◽  
Osamu Kozawa ◽  
Atsushi Suzuki ◽  
Yasuko Watanabe-Tomita ◽  
Yutaka Oiso ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Phospholipase D ◽  
Muscle Cells ◽  
Dependent Manner ◽  
Ang Ii ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle

Abstract In a previous study, we have shown that angiotensin II (Ang II) activates phosphatidylcholinehydrolyzing phospholipase D due to Ang II-induced Ca2+ influx from extracellular space in subcultured rat aortic smooth muscle cells. In the present study, we have investigated the role of phospholipase D in Ang II-induced arachidonic acid (AA) metabolite release and prostacyclin synthesis in subcultured rat aortic smooth muscle cells. Ang II significantly stimulated AA metabolite release in a concentration-dependent manner in the range between 1 nmol/l and 0·1 μmol/l. d,l-Propranolol hydrochloride (propranolol), an inhibitor of phosphatidic acid phosphohydrolase, significantly inhibited the Ang II-induced release of AA metabolites. The Ang II-induced AA metabolite release was reduced by chelating extracellular Ca2+ with EGTA. Genistein, an inhibitor of protein tyrosine kinases, significantly suppressed the Ang II-induced AA metabolite release. 1,6-Bis-(cyclohexyloximinocarbonylamino)-hexane (RHC-80267), a potent and selective inhibitor of diacylglycerol lipase, significantly inhibited the Ang II-induced AA metabolite release. Both propranolol and RHC-80267 inhibited the Ang II-induced synthesis of 6-keto-prostaglandin F1α, a stable metabolite of prostacyclin. The synthesis was suppressed by genistein. These results strongly suggest that the AA metabolite release induced by Ang II is mediated, at least in part, through phosphatidylcholine hydrolysis by phospholipase D activation in aortic smooth muscle cells. European Journal of Endocrinology 136 207–212

Adrenomedullin inhibits angiotensin II-induced contraction in human aortic smooth muscle cells

2006 ◽  
Vol 133 (1-3) ◽  
pp. 155-159 ◽  
Author(s):  
Fabio Rossi ◽  
Catia Zappa ◽  
Antonella Ferraresi ◽  
Vittorio Santiemma
Keyword(s):  
Smooth Muscle ◽  
Angiotensin Ii ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Aortic Smooth Muscle Cells ◽  
Aortic Smooth Muscle
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