Perinatal taurine exerts a hypotensive effect in male Spontaneously Hypertensive Rats and down-regulates endothelial Oxide Nitric Synthase in the aortic arch

Abstract

Essential hypertension is considered to be a result of the interaction between genetic and environmental factors, including perinatal factors. Different advantageous perinatal factors proved to have beneficial long-lasting effects against an abnormal genetic background. Taurine is a ubiquitous sulphur-containing amino acid present in food. The antihypertensive effects of taurine have been reported in experimental studies and in human hypertension. We aimed to investigate in spontaneously hypertensive rats (SHR), a known model of genetic hypertension, whether taurine administration during pregnancy and lactation would influence 1) systolic blood pressure (SBP), 2) aortic geometry, and 3) cardiac hypertrophy in adult offspring. Additionally; we aimed to determine whether perinatal taurine administration is associated with changes in relative telomere length (RTL) and gene expression of target genes. Female SHR were administered with taurine (3 g/l) during gestation and lactation (SHR-TAU). Untreated SHR and Wistar-Kyoto rats (WKY) were used as controls. Long lasting effects in offspring were investigated. Addition of taurine to the mother?s drinking water improved SBP in adult offspring. No differences were observed in aortic morphometry or cardiac hypertrophy. We suggest that taurine programming albeit sex-specific, is associated with gene expression changes which ultimately may lead to improvement of aortic remodelling and enhanced endothelial function because of augmented nitric oxide production. Specifically, we found modifications in gene expression of Bcl-2 family members and upregulation of endothelial nitric oxide synthase in the aorta of 22-week-old male offspring. No differences were observed on RTL in different cardiovascular tissues between SHR and SHR-TAU. Although SHR have responded only moderately to perinatal treatment, our findings supports the possibility of improving the genetically hypertensive state by manipulating the early environment.