Increased exposure to sodium during pregnancy and lactation changes basal and induced behavioral and neuroendocrine responses in adult male offspring

LÚCIO-OLIVEIRA; RUGINSK, S; VIVAS, L; ANTUNES-RODRIGUES, J; MECAWI, A.S.; GREENWOOD, M.P; ELIAS, LK; SILVA, M; ALMEIDA, L.; GREENWOOD, M; MURPHY, D

Physiological Reports

Wiley Periodicals, Inc on behalf of The Physiological Society and the American Physiological Society.

Año: 2017 vol. 5 p. 1 - 13

2051-817X

Excessive sodium (Na+) intake in modern society has been associated withseveral chronic disorders such as hypertension. Several studies suggest thatearly life events can program physiological systems and lead to functionalchanges in adulthood. Therefore, we investigated behavioral and neuroendocrineresponses under basal conditions and after 48 h of water deprivationin adult (60-day-old Wistar rats) male, Wistar rats originating from damswere offered only water or 0.15 mol/L NaCl during pregnancy and lactation.Early life salt exposure induced kidney damage, as shown by a higher numberof ED-1 positive cells (macrophages/monocytes), increased daily urinary volumeand Na+ excretion, blunted basal water intake and plasma oxytocinlevels, and increased plasma corticosterone secretion. When challenged withwater deprivation, animals exposed to 0.15 mol/L NaCl during early lifeshowed impaired water intake, reduced salt preference ratio, and vasopressin(AVP) secretion. In summary, our data demonstrate that the perinatal exposureto excessive Na+ intake can induce kidney injury in adult offspring andsignificantly affect the key mechanisms regulating water balance, fluid intake,and AVP release in response to water deprivation. Collectively, these novelresults highlight the impact of perinatal programming on the homeostaticmechanisms regulating fluid and electrolyte balance during exposure to anenvironmental stress (i.e. dehydration) in later life