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Recent evidence supports a role for the gut microbiota in hypertension, but whether ambulatory blood pressure is associated with gut microbiota and their metabolites remains unclear. We characterized the function of the gut microbiota, their metabolites and receptors in untreated human hypertensive participants in Australian metropolitan and regional areas. Ambulatory blood pressure, fecal microbiome predicted from 16S rRNA gene sequencing, plasma and fecal metabolites called short-chain fatty acid, and expression of their receptors were analyzed in 70 untreated and otherwise healthy participants from metropolitan and regional communities. Most normotensives were female (66%) compared with hypertensives (35%, P <0.01), but there was no difference in age between the groups (59.2±7.7 versus 60.3±6.6 years old). Based on machine learning multivariate covariance analyses of de-noised amplicon sequence variant prevalence data, we determined that there were no significant differences in predicted gut microbiome α- and β-diversity metrics between normotensives versus essential or masked hypertensives. However, select taxa were specific to these groups, notably Acidaminococcus spp ., Eubacterium fissicatena, and Muribaculaceae were higher, while Ruminococcus and Eubacterium eligens were lower in hypertensives. Importantly, normotensive and essential hypertensive cohorts could be differentiated based on gut microbiome gene pathways and metabolites. Specifically, hypertensive participants exhibited higher plasma acetate and butyrate, but their immune cells expressed reduced levels of short-chain fatty acid-activated GPR43 (G-protein coupled receptor 43). In conclusion, gut microbial diversity did not change in essential hypertension, but we observed a significant shift in microbial gene pathways. Hypertensive subjects had lower levels of GPR43, putatively blunting their response to blood pressure-lowering metabolites.

Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. One of the main causes of IUGR is uteroplacental vascular insufficiency. Under these circumstances of chronic oxygen and nutrient deprivation, the growth-restricted fetus often displays typical circulatory changes, which in part represent adaptations to the suboptimal intrauterine environment. These fetal adaptations aim to preserve oxygen and nutrient supply to vital organs such as the brain, the heart, and the adrenals. These prenatal circulatory adaptations are thought to lead to an altered development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities. In this review, we discuss the alterations to cardiovascular structure, function, and control that have been observed in growth-restricted fetuses, neonates, and infants following uteroplacental vascular insufficiency. We also discuss the current knowledge on early life surveillance and interventions to prevent progression into chronic disease. Intrauterine growth restriction (IUGR) refers to the situation where a fetus does not grow according to its genetic growth potential. The main cause of IUGR in developed countries is uteroplacental vascular insufficiency (1), which drives the fetus to redistribute its cardiac output to preserve oxygen and nutrient supply to the brain, heart, and adrenals. Although these adaptive circulatory changes are beneficial during intrauterine life, they are thought to cause dysfunctional development of the cardiovascular system and "program" the fetus for life long cardiovascular morbidities (2). This is also known as the Developmental Origins of Health and Disease hypothesis, which postulates that insults during intrauterine and early postnatal development can permanently change the body's structure, function, and metabolism and influence susceptibility to adult noncommunicable diseases (2). Despite their increased risk of cardiovascular disease, infants born growth restricted usually do not receive long-term cardiovascular follow-up. Depending on the definition used, IUGR can occur in up to 10% of pregnancies, and as cardiovascular disease is the number one cause of death worldwide (3), early identification of cardiovascular risk factors and targeted interventions in this high-risk population are of major clinical importance. In this review, we discuss the alterations of cardiovascular structure, function, and control that have been observed in infants born growth restricted and their implications for surveillance and intervention to prevent progression into chronic disease. CHALLENGES IN IDENTIFYING IUGRThe current literature uses many different definitions of IUGR, which may explain some of the contradicting findings discussed in this review. Traditionally, and most commonly, IUGR is defined as a birth weight below the 10th percentile for gestational age on the normative population growth curve (4). This definition, however, merely describes those who ...

In sleeping infants, sympathetic vascular modulation of the circulation decreases with age, while parasympathetic control of heart rate is strengthened. These normative data will aid in the early identification of conditions where autonomic function is impaired, such as in SIDS.

In healthy infants cerebral oxygenation is reduced during sleep in the prone position. This reduction may underpin the reduced arousability from sleep exhibited by healthy infants who sleep prone, a finding that provides new insight into potential risks of prone sleeping and mechanisms of sudden infant death syndrome.

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Moderate-severe OSA in preschool children has a significant effect on pulse transit time during REM sleep, indicating that these young children have a higher baseline BP during this state. We propose that the REM-related elevation in BP may be the first step toward development of daytime BP abnormalities. Given that increased BP during childhood predicts hypertension in adulthood, longitudinal studies are needed to determine the effect of resolution of snoring and/or OSA at this age.