The effect of chronic nitric oxide inhibition on vascular reactivity and blood pressure in pregnant rats
Takiuti, Nilton Hideto; Carvalho, Maria Helena Cetelli; Kahhale, Soubhi; Nigro, Dorothy; Barbeiro, Hermes Vieira; Zugaib, Marcelo.
São Paulo med. j
; 117(5): 197-204, Sept. 1999. tab, graf
Artigo
em Inglês
| LILACS | ID: lil-250191
CONTEXT The exact mechanism involved in changes in blood pressure and peripheral vascular resistance during pregnancy is unknown.
OBJECTIVE:
To evaluate the importance of endothelium-derivated relaxing factor (EDRF) and its main component, nitric oxide, in blood pressure and vascular reactivity in pregnant rats.DESIGN:
Clinical trial in experimentation animals.SETTING:
University laboratory of Pharmacology. SAMPLE Female Wistar rats with normal blood pressure, weight (152 to 227 grams) and age (90 to 116 days). INTERVENTION 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. MAIN MEASUREMENTS 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.RESULTS:
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.CONCLUSION:
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.
Biblioteca responsável:
BR1.1
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