Aim: 

C-type natriuretic peptide (CNP) is known to play a role in thelocal regulation of vascular tone but the role of this peptide in endothelial cells remains to be elucidated. The study investigates the effects of CNP on HUVECs and the interaction between CNP and Angiotensin II (Ang II) signalling pathways.

Methods: 

Cell migration by Boyden chambers is estimated by chemotactic factors as CNP (10-6M) and Ang II (10-7M) and with or without addition of L-NAME (1mM, NOS inhibitor), SNAP (10.4 M, NO donor) 8Br-cGMP (100 10-6M, PKG activator), Rp-8Br-Pet-cGMPs (100 10-6M, PKG inhibitor). The data evaluation is at 3, 6 hours. The images were captured by ProImagePlus on Olympus IX 50 microscope and their analysis was performed by NIH imageJ 1.6.2 program.Results: the data demonstrate that CNP , after treatment lag phase of either less than 24h or more than 48h, inhibits migratory activity of HUVECs in culture. This effect is modulated by either inhibiting or activating guanylate cyclase. Short lived NO generator SNAP acts against CNP 10-6 M, but SNAP alone at 10-4 M after 48h is always inhibitor of HUVEC migration down to control level, decreasing partially CNP 10-6 action. These observations demonstrate the limited effect of NO generation at 6 hours by SNAP 10-4 M . So CNP 10-6 M prevailing action is partially explained by the different kinetics of NO depletion and CNP action on HUVEC migration in cultures.

Researches in progress at intermediate timecourses shall verify the hypothesis.