Aim: 

Angiotensin II (Ang II) regulates the Atrial Natriuretic Peptide and Brain Natriuretic Peptide levels in cardiac cells, but its action at the C-Type Natriuretic Peptide level is not clear. We examined whether Ang II induced significant modulation of CNP levels in human umbilical vein endothelial cells (HUVECs) and the involvement of the voltage operated calcium channel expressed in the endothelial cell: T-Type calcium channel (TCC) and L-Type calcium channel (LCC). We further investigated the role of AT1 receptor in this mechanism.

Methods: 

The HUVECs were treated with Ang II either 10^-6M, or 10^-7M or 10^-9M in the presence of calcium channel blockers either mibefradil 10^-5M or verapamil 10^-7M, respectively selective for TCC and LCC; PD123319 10^-7M as AT2 Receptor antagonist. The CNP protein was probed by immunostaining in the same cultures.

Results: 

The immunofluorescence method reveals that Ang II at 10^-6M and 10^-7M increases significantly the CNP levels for long term in the HUVECs; Ang II 10^-9M induces the same effect but loses gradually the biological power as function of time, in fact after 48 h the CNP secretion is reduced.

Conclusions: 

Ang II modulates positively the CNP secretion into the vascular endothelial cell and that effect is more relevant after 24-48h. The treatment with PD123319 points out that Ang II mediated the modulation of CNP levels via AT1R and involving both voltage calcium channels, TCC and LCC.