Fig. 2.

Nitric oxide-dependent vasodilation in the placenta. Vasodilator effects of NO in placental vessels can be induced via; a) activation of protein kinases (i.e. PKC, Akt and ERK1/2) by shear stress (SS), adenosine (Ado), ATP, VEGF or PlGF; and b) increasing intracellular calcium concentration induced by agonists (i.e. CGRP and histamine). Both pathways activate eNOS leading to NO production, which diffuses to the adjacent smooth muscle layer. Noteworthy, NO action on placental smooth muscle cells occurs either in a cGMP-dependent (PKG) and -independent (BK_Ca) fashion.