Previous experiments demonstrate that over or under exposure to taurine from conception until weaning (perinatal life) alters long-term regulation of renal function and arterial pressure . The present study demonstrates that both prenatal and postnatal taurine manipulation can impair renal function in adult male rats. Prenatal taurine supplementation and postnatal taurine deficiency had many similar adverse effects on the adult renal function, including decreased renal blood flow and resting water and sodium excretion, and increased renal vascular resistance and resting tubular sodium reabsorption. However, both prenatal and postnatal taurine supplementation markedly blunted renal pressure-diuresis/natriuresis in the adult.
Prenatal taurine deficiency produces low birth weight in animals, especially cats. These animals also display many abnormalities including organ damage [2, 3, 12]. The only difference in organ weights in the current study was the slight increase in heart weight in TDF. These data indicate that the taurine manipulations shortly during prenatal or postnatal period do not dramatically alter growth of the animal or compromise overall organ growth. Further, heart rates were not different among groups, indicating that the taurine manipulations do not have a gross effect on this parameter; however, whether cardiac contractility and/or stroke volume differ among groups should be directly tested in the future.
In rats, nephrogenesis is completed before birth, but renal differentiation and maturation continue postnatally [14, 15]. In the present study, postnatal taurine deficiency impairs renal function especially renal hemodynamics and resting water and sodium excretion slightly greater than prenatal deficiency. This suggests that taurine exposure has a significant role in the development of renal function in early postnatal life. In the present study, all rats were supplied by a normal rat food from weaning to the end of experiment, thus, the changes in the pre and postnatal taurine deficient rats was not fully corrected by post-weaning normalization of taurine in the diet. In the present study, prenatal (compared to postnatal) taurine-depleted rats displayed relatively minor deficits in renal blood flow and sodium excretion, suggesting that postnatal taurine exposure may partially restore renal function in these rats.
Our previous study demonstrates that perinatal taurine deficiency depresses autonomic nervous system function in adult male rats and that this can be reversed by high sugar intake post-weaning . This suggests that an early life dietary intervention can reverse renal deficits attributable to taurine deficiency.
Our previous data demonstrates that perinatal taurine depletion from conception until weaning does not alter arterial pressure or heart rate in adult male and increases arterial pressure but not heart rate in female rats. In addition, high sugar intake induces hypertension only in male rats . The present data extend these findings, demonstrating that selective prenatal or postnatal taurine deficiency has no long-term effect on arterial pressure and heart rate at this stage of adult life. However, taurine contributes importantly to nervous system growth and differentiation [3, 17, 18], and abnormal autonomic nervous system function underlines sugar-induced hypertension in perinatal taurine-depleted male rats . In addition, high dietary sugar be itself does not increase arterial pressure in most studies. Thus, altered, early-life taurine exposure may be a co-factor for other hypertensive agents and thereby contribute to hypertension. Sympathetic nervous system overactivtiy also directly impacts target organs and/or indirectly affects them via other mechanisms, e.g., the renin-angiotensin system.
Long-term arterial pressure control is mainly dependent on renal pressure-diuretic/natriuretic mechanisms [19–21]. In general, the kidneys will excrete sufficient water and sodium to reduce arterial pressure to normal levels. In the present study, water and sodium excretion in responses to an acute saline load were not significantly different among groups despite higher arterial pressures in perinatal taurine-supplemented groups, suggesting that blunted renal pressure-diuretic/natriuretic mechanisms are present in this group as well as the taurine-depleted groups.
Perinatal malnutrition and low birth weight can lead to adult hypertension, renal dysregulation, obesity, diabetes mellitus and other abnormalities . These early life abnormalities appear to cause cell adaptation that prefers anabolism over catabolism in adults. Without a sufficient diet and activity control, such individuals are at higher risk of obesity, hypertension, and other cardiovascular diseases. Although obesity and insulin resistance  were not observed in the present animals, renal dysregulation was confirmed. Further, the present data suggest that if these animals were studied when aged (e.g., 12 months or beyond), early deficits in renal, glucose/insulin and autonomic dysregulation may lead to insulin resistance, diabetes, and hypertension.
During pregnancy, mothers need more nutrients for their own lives and their fetuses. Many commercial dietary supplements contain sufficient taurine for these individuals [9, 23, 24], and taurine plays many physiological roles throughout life. Our previous studies indicate that taurine supplementation from conception until weaning significantly increases arterial pressure and renal vascular resistance and decreases renal blood flow in adult female rats . The present study further demonstrates that both prenatal and postnatal taurine over exposure contributes to similar effects in male rats. Prenatal over nutrition has also been reported to induce obesity and hypertension in the elderly [25–27], and the current data indicate that excess taurine may have some adverse side effects.