Abstract
Nitric oxide (NO) deficiency during pregnancy is a key reason for preeclampsia development. Besides its important vasomotor role, NO is shown to regulate the cell transcriptome. However, the role of NO in transcriptional regulation of developing smooth muscle has never been studied before. We hypothesized that in early ontogeny, NO is important for the regulation of arterial smooth muscle-specific genes expression. Pregnant rats consumed NO-synthase inhibitor L-NAME (500 mg/L in drinking water) from gestational day 10 till delivery, which led to an increase in blood pressure, a key manifestation of preeclampsia. L-NAME reduced blood concentrations of NO metabolites in dams and their newborn pups, as well as relaxations of pup aortic rings to acetylcholine. Using qPCR, we demonstrated reduced abundances of the smooth muscle-specific myosin heavy chain isoform, α-actin, SM22α, and L-type Ca2+-channel mRNAs in the aorta of newborn pups from the L-NAME group compared to control pups. To conclude, the intrauterine NO deficiency weakens gene expression specific for a contractile phenotype of arterial smooth muscle in newborn offspring.
Highlights
Nitric oxide (NO) is one of the most important regulatory molecules in the cardiovascular system
The bodyweight of females consuming L-NAME did not differ from the weight of control females throughout pregnancy (Figure 1a)
The daily relative water consumption throughout the pregnancy did not differ between control and L-NAME
Summary
Nitric oxide (NO) is one of the most important regulatory molecules in the cardiovascular system. NO is produced by the vascular endothelium and has a potent vasodilatory effect. There are three isoforms of the enzyme that synthesizes NO: endothelial, neuronal, and inducible NO synthases (eNOS, nNOS, and iNOS, respectively). The endothelial isoform of the enzyme predominates in the vascular endothelium [1,2]. The production of NO by the endothelium can undergo significant changes during early ontogenesis in different regions of the vascular bed. In the early postnatal period, the contribution of NO to the regulation of vascular tone is large in the gastrointestinal tract, skin, the preglomerular arterioles of the kidney, and skeletal muscle feed arteries [1,3]
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