Abstract
The exact mechanism involved in changes in blood pressure and peripheral vascular resistance during pregnancy is unknown. To evaluate the importance of endothelium-derived relaxing factor (EDRF) and its main component, nitric oxide, in blood pressure and vascular reactivity in pregnant rats. Clinical trial in experimentation animals. University laboratory of Pharmacology. Female Wistar rats with normal blood pressure, weight (152 to 227 grams) and age (90 to 116 days). The rats were divided in to four groups: pregnant rats treated with L-NAME (13 rats); pregnant control rats (8 rats); virgin rats treated with L-NAME (10 rats); virgin control rats (12 rats). The vascular preparations and caudal blood pressure were obtained at the end of pregnancy, or after the administration of L-NAME in virgin rats. The caudal blood pressure and the vascular response to acetylcholine in pre-contracted aortic rings, both with and without endothelium, and the effect of nitric oxide inhibition, Nw-L-nitro-arginine methyl-ester (L-NAME), in pregnant and virgin rats. The L-NAME was administered in the drinking water over a 10-day period. The blood pressure decreased in pregnancy. Aortic rings of pregnant rats were more sensitive to acetylcholine than those of virgin rats. After L-NAME treatment, the blood pressure increased and relaxation was blocked in both groups. The fetal-placental unit weight of the L-NAME group was lower than that of the control group. Acetylcholine-induced vasorelaxation sensitivity was greater in pregnant rats and that blood pressure increased after L-NAME administration while the acetylcholine-induced vasorelaxation response was blocked.
Highlights
Various hemodynamic changes characterized by decreased, systemic, vascular resistance and decreased blood pressure are associated with pregnancy.[1,2,3,4] The exact physiopathological mechanisms by which these vascular changes take place are not known
Nitric oxide is known to be the principal component in endotheliumderivated relaxing factor (EDRF), which is released by acetylcholine stimulus.[7,8,9]
Nitric oxide acts by stimulating soluble guanylate cyclase resulting in an increase in the intracellular concentration of cyclic guanosine monophosphate in the smooth muscle cells, which leads to vasorelaxation.[12,13,14]
Summary
Various hemodynamic changes characterized by decreased, systemic, vascular resistance and decreased blood pressure are associated with pregnancy.[1,2,3,4] The exact physiopathological mechanisms by which these vascular changes take place are not known. Many factors such as decreased blood viscosity, changes in the prostacyclin/thromboxane ratio and a decrease in nitric oxide activity or synthesis are involved.[5, 6]. Nitric oxide is known to be the principal component in EDRF (endotheliumderivated relaxing factor), which is released by acetylcholine stimulus.[7,8,9] This nitric oxide is produced by the vascular endothelium and it regulates the vascular vasorelaxation tonus and blood pressure.[10,11] Nitric oxide acts by stimulating soluble guanylate cyclase resulting in an increase in the intracellular concentration of cyclic guanosine monophosphate in the smooth muscle cells, which leads to vasorelaxation.[12,13,14]
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