Objective: We attempted to investigate the role of nitric oxide(NO) in pathogenesis of pregnancy-induced hypertension(PIH).
Methods: No-nitro-L-arginine-methyl ester(L-NAME) was used to inhibit nitric oxide synthase(NOS) in pregnant rats. Indices including blood pressure, urine protein concentration, pup weight, serum NO level and plasma ET-1 level were measured. Nitroglycerin, a nitric oxide donor, was used to observe its impact on the effect of L-NAME at the same time.
Results: Infusion of L-NAME elevated blood pressure, increased urine protein concentration, decreased pup weight, decreased serum NO level and raised plasma ET-1 level(P < 0.01, respectively); However in the L-NAME-treated animals nitroglycerin significantly lowered blood pressure, decreased urine protein concentration, increased pup weight, increased serum NO level and decreased plasma ET-1 level(P < 0.01, respectively).
Conclusions: 1. Infusion of L-NAME, an inhibitor of NOS, causes decreased serum NO level and some signs similar to preeclampsia such as hypertension, proteinuria and intrauterine growth retardation(IUGR). Nitroglycerin can reverse the lesions induced by the treatment of L-NAME. These findings indicate that reduced level of NO may be a factor responsible for PIH. 2. NO can decrease the plasma ET-1 level. NO may regulate the process of PIH via ET-1 pathway. It may be one mechanism for NO. 3. An useful animal model for PIH is provided to test novel therapeutic and preventive strategies.