Differential expression of renal nitric oxide synthase isoforms during pregnancy in rats

Citation
Bt. Alexander et al., Differential expression of renal nitric oxide synthase isoforms during pregnancy in rats, HYPERTENSIO, 33(1), 1999, pp. 435-439
Citations number
29
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194-911X → ACNP
Volume
33
Issue
1
Year of publication
1999
Part
2
Supplement
S
Pages
435 - 439
Database
ISI
SICI code
0194-911X(199901)33:1<435:DEORNO>2.0.ZU;2-V
Abstract
Alterations in nitric oxide (NO) production have been suggested to play a r ole in mediating changes in renal function during normal pregnancy and in p regnancy-induced hypertension. Although NO production is enhanced during no rmal pregnancy, the mechanisms for the increase are unknown. The purpose of this study was to determine whether the elevation in NO production during pregnancy is associated with increases in renal expression of endothelial ( eNOS), inducible (iNOS), and neuronal (nNOS) nitric oxide syntheses. To ach ieve this goal we examined systemic and renal hemodynamics, urinary excreti on of nitrate/nitrite, and renal protein expression of the three NOS isofor ms in prepregnant rats, pregnant rats at days 6, 13, and 19 of gestation an d at day 4 postpartum. Mean arterial pressure decreased by 14% in late preg nancy whereas the glomerular filtration rare and renal plasma flow increase d by 21% and 24%, respectively, in mid pregnancy. Excretion of nitrate/nitr ite increased throughout pregnancy with a 3.4-fold increase present at day 19 (12.2+/-0.7 to 41.1+/-1.3 mu mol/24 h). Renal eNOS protein expression de creased by 39% during pregnancy with the lowest level resulting at day 19 a nd returning to virgin levels by day 4 post partum. In contrast, renal iNOS and nNOS protein expression increased 31% and 25%, respectively, with high est expression occurring for both at day 13 of pregnancy. These data sugges t that the increased NO production and renal hemodynamics associated with p regnancy in rats may be caused by the upregulation of iNOS and nNOS in the kidney.