Lysophosphatidylcholine triggers intracellular calcium release and activation of non-selective cation channels in renal arterial smooth muscle cells

2000 ◽  
Vol 439 (4) ◽  
pp. 495-500 ◽  
Author(s):  
R. I. Jabr ◽  
J. Yamazaki ◽  
J.R. Hume
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Muscle Cells ◽  
Cation Channels ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Intracellular Calcium Release

Effects of kinins on cultured arterial smooth muscle

1990 ◽  
Vol 258 (2) ◽  
pp. C299-C308 ◽  
Author(s):  
B. S. Dixon ◽  
R. Breckon ◽  
J. Fortune ◽  
R. J. Vavrek ◽  
J. M. Stewart ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Intracellular Calcium ◽  
Muscle Cells ◽  
Mesenteric Arteries ◽  
Cellular Mechanisms ◽  
Response Curves ◽  
Arterial Smooth Muscle ◽  
Arterial Smooth Muscle Cells ◽  
Pg E2

The present study uses various kinin agonists and antagonists to examine the cellular mechanisms of bradykinin's actions on intracellular calcium, prostaglandins, and adenosine 3',5'-cyclic monophosphate (cAMP) accumulation in cultured arterial smooth muscle cells (casmc) obtained from rat mesenteric arteries. Exposure to bradykinin produced a rapid release of calcium (peak less than or equal to 20 s) from intracellular stores and an increase in prostaglandin (PG) E2 and cAMP production in casmc. Compared with bradykinin, the bradykinin B1-agonist [des-Arg9]BK produced only a small increase in intracellular calcium. The bradykinin-mediated increase in intracellular calcium was competitively blocked by the B2 receptor antagonist [D-Arg-O-Hyp3-Thi5,8-D-Phe7]BK (B4307) but not the B1-antagonist ([des-Arg9-Leu8]BK). In addition, the similarity of the dose-response curves for the bradykinin-mediated increase in Ca2+, PGE2, and cAMP (half-maximal stimulation of 12, 11, and 13 nM, respectively) and the ability of the B2-antagonist (B4307) to block each of these effects of bradykinin suggest that all three effects are mediated by the same bradykinin (B2) receptor. Further studies revealed that increases in intracellular calcium are necessary for the bradykinin-mediated increase in PGE2 formation and the subsequent PGE2-dependent formation of cAMP. Taken together, these results suggest that bradykinin acts via a B2-receptor on arterial smooth muscle cells to release calcium from intracellular stores, leading to increases in PGE2 production and the PGE2-dependent activation of adenylate cyclase.

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