[Nitric oxide as a regulator of hemodynamic changes in pregnancy]

Nitric oxide (.NO) produced by the majority of animal cells, has been considered a second messenger, since it is the result of a transduction process induced by a first stimulus. Biochemically, .NO is produced during the conversion of L-arginine to L-citruline by a reaction catalyzed by the enzyme nitric oxide synthetase. Two ixoenzymes have been characterized from this enzyme: a constitutive isoenzyme activated by hormones produced by the endothelial cells and acting on smooth muscle relaxing properties and the other, an inducible isoenzyme whose synthesis is stimulated by cytokines, and produced by macrophages. As pregnancy progresses, the concentrations of .NO, its metabolites, nitrates and nitrites, cGMP and the synthesizing enzyme, nitric oxide synthetase, increase parallelly until reaching a maximum peak before birth. It is considered that .NO is the molecule that maintains the typical vasodilated tone during pregnancy. During preeclampsia, this free radical, as well as its metabolites are found to be significantly decreased, in addition, the administration of .NO donors or of the precursor of L-arginine reverts the vascular abnormalities of this condition. The mechanism of action behind .NO on the vascular endothelium is by its stimulating effect on the enzyme cyclase guanilate, causing an increase in cGMP concentration and the relaxation of the smooth muscle. The nitric oxide generates by macrophages acts as a defense mechanism when linked with other radicals as the superoxide anion (O2).