Changes in endothelial nitric oxide production in systemic vessels during early ontogenesis—A key mechanism for the perinatal adaptation of the circulatory system

Abstract

Nitric oxide (NO) produced in the wall of blood vessels is necessary for the regulation of vascular tone to ensure an adequate blood supply of organs and tissues. In this review, we present evidence that the functioning of endothelial NO-synthase (eNOS) changes considerably during postnatal maturation. Alterations in NO-ergic vasoregulation in early ontogeny vary between vascular beds and correlate with the functional reorganization of a particular organ. Importantly, the anticontractile effect of NO can be an important mechanism responsible for the protectively low blood pressure in the immature circulatory system. The activity of eNOS is regulated by a number of hormones, including thyroid hormones which are key regulators of the perinatal developmental processes. Maternal thyroid hormone deficiency suppresses the anticontractile effect of NO at perinatal age. Such alterations disturb perinatal cardiovascular homeostasis and lead to delayed occurring cardiovascular pathologies in adulthood. The newly discovered role of thyroid hormones may have broad implications in cardiovascular medicine, considering the extremely high prevalence of maternal hypothyroidism in human society.