[Effect of knockout AT1a receptor gene on transplasmamembrane calcium influx in aortic smooth muscle cells].
OBJECTIVE
To investigate the mechanism of angiotensin II receptor subtype (AT1a) mutant on angiotensin II (Ang II) mediated transplasmamembrane calcium influx in aortic smooth muscle cells (SMCs) from AT1a knockout and wild type mice.


METHODS
Aortic SMCs were isolated and cultured. Intracellular free calcium concentration [Ca2+]i was measured using Fura-2/AM fluorescentic technique.


RESULTS
Ang II caused a marked increase in [Ca2+]i in both cell types [AT1a group: (204 +/- 22) nmol/L vs (108 +/- 9) nmol/L];


METHODS
[(194 +/- 19) nmol/L vs (110 +/- 7) nmol/L]. Administration of both calcium channel blocker, nifedipine and GTP-gamma s significantly inhibited Ang II effect, in contrast, application of pertussin toxin (PTX) activated the Ang II mediated calcium influx. The response of AT1a knockout cells was more sensitive to nifedipine and were enhanced by PTX.


CONCLUSIONS
Calcium influx induced by Ang II can be regulated by PTX insensitive and non-Gi protein in AT1a knockout cells.
Zhu
Z
Z
Hypertension Center, Daping Hospital, Third Military Medical University, Chongqing 400042.
Zhu
S
S
Hu
H
H
D000818:Animals; D001011:Aorta / Q000166:cytology; D001693:Biological Transport, Active; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D051379:Mice; D018345:Mice, Knockout; D009131:Muscle, Smooth, Vascular / Q000166:cytology / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics*
D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D002118:Calcium