Aim: 

The CNP is component of natriuretic peptide family and have an important role in regulation of vascular tone. Is known the involvement of Ang II to release ANP and BNP in cardiac cell but not in the CNP release. We examined whether Ang II modulate CNP levels in human umbilical vein endothelial cells (HUVECs) and the contribution of the voltage operated calcium channel expressed in the endothelial cell: T-Type calcium channel (TCC) and L-Type calcium channel (LCC) which regulates the protein release. We further investigated the role of AT1 and AT2 receptors in this mechanism.

Methods: 

The HUVECs were treated with Ang II at 10^-7M in the presence of calcium channel blockers, either mibefradil 10^-5M or verapamil 10^-7M, respectively selective for TCC and LCC; The contribution of Ang II receptors is evaluated using PD123319 10^-7M, (AT2 Receptor antagonist) and ZD 7155 10^-7M (AT1 Receptor antagonist). The CNP protein was probed by immunostaining in same cultures.

Results: 

The immunofluorescence method reveals that ang II increases CNP levels for long term in the HUVECs; the AT1R blockade is necessary to observe significant increase of CNP_.levels. Pretreatment with mibefradil abolishes the Ang II–induced CNP release.

Conclusions: 

Ang II modulates positively the CNP secretion into the vascular endothelial cell.The only treatment with ZD 7155 points out that Ang II mediated the modulation of CNP levels activating AT2R pathway and both voltage calcium channel: TCC and LCC.