Prenatal high-salt diet in the Sprague-Dawley rat programs blood pressure and heart rate hyperresponsiveness to stress in adult female offspring

Abstract

Porter JP, King SH, Honeycutt AD. Prenatal high-salt diet in the Sprague-Dawley rat programs blood pressure and heart rate hyperresponsiveness to stress in adult female offspring. Am J Physiol Regul Integr Comp Physiol 293: R334-R342, 2007. First published May 9, 2007; doi:10.1152/ajpregu.00887.2006.-Several animal models have been developed to study fetal programming of hypertension. One model involves feeding high-salt (HS) diet to rats before and during pregnancy, during lactation, and after weaning for 10 days. In the present investigation, we limited HS diet to the prenatal period in an attempt to find a narrower critical window for fetal programming. The HS diet did not result in low-birth weight offspring. In the adult offspring, radiotelemetry was used to assess blood pressure and heart rate in the conscious unstressed state. As adults, the HS offspring were not hypertensive compared with normal-salt (NS) control animals. However, the pressor and tachycardic responses to 1-h of restraint were significantly enhanced in HS female offspring, and recovery after restraint was delayed. This was accompanied by an increase in relative expression of corticotropin-releasing hormone (CRH) mRNA in the paraventricular nucleus of the hypothalamus during basal and stressed conditions. There was no augmented stress response or relative increase in CRH mRNA in adult HS male offspring. When challenged with 1 wk of 8% NaCl diet as adults, neither HS male nor female offspring exhibited salt sensitivity compared with NS groups. These data show that a high-salt diet limited to the prenatal period is not sufficient to program hypertension in adult offspring. However, this narrower critical period is sufficient to imprint a lasting hyperresponsiveness to stress, at least in adult female offspring. These data indicate that excessive maternal salt intake during pregnancy can adversely affect the cardiovascular health of adult offspring. corticotropin-releasing hormone; paraventricular nucleus; hypertension; radiotelemetry; sodium chloride; pregnancy; prenatal nutrition physiology IN RECENT YEARS, SEVERAL ANIMAL models have been developed to study developmental origins (also known as fetal programming) of adult diseases, including hypertension. Most of these have been models of low birth weight in an attempt to better understand clinical data in humans that suggest low birth weight is associated with hypertension in later life. Of these, the protein undernutrition model has received the most attention. Limiting maternal protein intake during pregnancy produces small offspring in rats. These offspring are hypertensive as adults (24,31,45). Another model has used ligation of the uterine arteries to produce underperfusion of the placenta. Offspring are small and develop hypertension as adults (1, 36). A third model involves injection of dexamethasone into pregnant animals near parturition. Once again, offspring are small and develop hypertension later in life (11, 44). All of these models provide evidence that the fetal environment...

Antenatal excessive sodium intake induces adverse vascular remodelling in offspring

“…In addition, blood pressure was not different between the groups of offspring, nor between the groups of dams at the end of pregnancy. The lack of effect of high salt intake during pregnancy on blood pressure in the offspring is remarkable, although Porter et al [13] obtained similar results in previous studies. Interestingly, the latter study did reveal an increased blood pressure response to stress in the offspring.…”

Sex differences in the developmental origins of hypertension and cardiorenal disease

“…A high-salt diet during pregnancy in rats has also been evaluated and reported to alter the response to restraint stress in female offspring. Further, female high-salt diet offspring had increased corticotrophinreleasing hormone mRNA levels in the PVN than did normalsalt diet females (98).…”

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“…Prenatal growth is sensitive to the direct and indirect effects of maternal dietary intake; manipulation of maternal diet can lead to behavioural and physiological changes of the offspring later in life. Offspring of mothers with excess intake of salt develops higher than average blood pressure in adulthood [4,5]. High salt intake in weanling DS rats modified cataract formation in association with hypertension [6].…”