NDLI: Changes of intracellular calcium concentrations by phenylephrine in renal arterial smooth muscle cells

Content Provider	Springer Nature Link
Author	Utz, J. Eckert, R. Trautwein, W.
Abstract	In smooth muscle cells isolated from swine renal interlobar arteries, phenylephrine (PE) at concentrations of 1–10 µM produced biphasic increases of the intracellular calcium concentration. An early transient rise was followed by a maintained plateau. The maintained component was sensitive to extracellular calcium, in contrast to the early transient, which was still observed in nominally calcium-free solution. Nifedipine (1 µM) and NiCl2 (100 µM) only weakly affected the calcium signal, suggesting that voltage-sensitive calcium channels play only a minor role in the PE-induced changes in intracellular calcium. Thapsigargin (0.5 µM) elevated the intracellular calcium concentration and depressed both the early transient and the maintained component of the PE response. In calcium-free medium PE induced a transient rise of the intracellular calcium concentration with a depressed plateau. Readmission of calcium elevated the intracellular calcium concentration above the baseline. Both components of the PE-induced calcium signal were completely abolished when the cells were pretreated with the phospholipase C (PLC) inhibitor U73122 (2 µM). LaCl3 (100 µM, 1 mM), an inhibitor of calcium-release-activated current (I CRAC), had no effect on the PE-induced calcium signal. GdCl3 (50 µM), SKF 96365 (10 µM) and flufenamic acid (100 µM), reported to inhibit nonselective cation channels, blocked or transiently reduced the maintained calcium signal. Several protein kinase inhibitors such as genistein (10 µM), H7 (50 µM), H89 (1 µM) and bisindolylmaleimide (0.2 µM) reduced the maintained calcium signal. We conclude that the initial transient spike of the PE-induced calcium signal is due to release of calcium from inositol 1,4,5-trisphosphate-sensitive calcium stores evoked by α1-adrenoceptor-coupled stimulation of PLC and that the maintained component is due to capacitative calcium entry, which is modulated by protein kinases.
Starting Page	725
Ending Page	731
Page Count	7
File Format	PDF
ISSN	00316768
Journal	Pflügers Archiv
Volume Number	438
Issue Number	6
e-ISSN	14322013
Language	English
Publisher	Springer-Verlag
Publisher Date	1999-09-07
Publisher Place	Berlin, Heidelberg
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Clinical Biochemistry

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