Abstract
Nitric oxide (NO) has been shown to stimulate differentiation and increase the survival of ganglionic sympathetic neurons. The proportion of neuronal NOS-immunoreactive sympathetic preganglionic neurons is particularly high in newborn rats and decreases with maturation. However, the role of NO in the development of vascular sympathetic innervation has never been studied before. We tested the hypothesis that intrauterine NO deficiency weakened the development of vascular sympathetic innervation and thereby changed the contractility of peripheral arteries and blood pressure level in two-week-old offspring. Pregnant rats consumed NOS inhibitor L-NAME (250 mg/L in drinking water) from gestational day 10 until delivery. Pups in the L-NAME group had a reduced body weight and blood level of NO metabolites at 1–2 postnatal days. Saphenous arteries from two-week-old L-NAME offspring demonstrated a lower density of sympathetic innervation, a smaller inner diameter, reduced maximal active force and decreased α-actin/β-actin mRNA expression ratio compared to the controls. Importantly, pups in the L-NAME group exhibited decreased blood pressure levels before, but not after, ganglionic blockade with chlorisondamine. In conclusion, intrauterine L-NAME exposure is followed by the impaired development of the sympathetic nervous system in early postnatal life, which is accompanied by the structural and functional remodeling of arterial blood vessels.
Highlights
The body weights of females in the control group and L-NAME group were almost similar at the seventh gestation day (GD7, Figure 1a)
To identify whether Nitric oxide (NO) deficiency affects the development of sympathetic innervation, we evaluated the density of adrenergic fiber plexus in isolated saphenous arteries in twoweek-old pups
We have shown that saphenous arteries from two-week-old L-NAME offspring have a smaller inner diameter and maximum contractility, the latter often correlating with reduced media thickness [47]
Summary
Nitric oxide (NO) is an important regulatory molecule in mammalian organisms. Relevant NO is generated by two constitutive nitric oxide synthase isoforms: neuronal (nNOS) and endothelial (eNOS) [1,2]. The regulation of the circulatory system has many unique characteristics compared to adult organisms, one of which is the augmented role of NO in vasomotor control [2,4]. Such a high level of NO production/action is important for maintaining low blood pressure in the developing cardiovascular system [5,6] and preventing the overstretching of and damage to the immature heart and vasculature
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