Impact of perinatal hypertonic NaCl access on adult offspring's sodium intake and angiotensin and vasopressin systems under hypertension model.

Perinatal natriophilia has programming effects on blood pressure control, inducing anatomical and molecular changes in the kidney and brain that impair blood pressure reestablishment after a pressor challenge, such as an osmotic stimulation. However, the imprinted effect of voluntary sodium consumption during this period on the development of hypertension is unclear. To evaluate this, we studied the effect of deoxycorticosterone acetate and high-salt diet (DOCA-salt) treatment on blood pressure and sodium intake responses, and gene expression in the kidney and brain in adult offspring exposed to voluntary hypertonic sodium consumption during the perinatal period (PM-NaCl group). Male PM-NaCl rats consumed more sodium than controls (PM-Ctrol group) during DOCA treatment. However, the hypertension induced did not differ between the PM-NaCl and PM-Ctrol groups. This behavioral change was accompanied by a higher angiotensin type 1 receptor (Agtr1a) gene expression at brain level in the subfornical organ and the hypothalamic paraventricular nucleus of PM-NaCl, areas key to the modulation of salt appetite and autonomic function. At renal level, programmed animals showed differing responses in gene expression induced by DOCA-salt treatment compared to the PM-Ctrol group, such as expression of Agtr1a, transient receptor potential vanilloid type 1 channel in the medulla and vasopressin 2 receptor in the renal cortex. The data indicates that the availability of a rich source of sodium during the perinatal period induces a long-term effect in DOCA-salt treated rats, modifying behavioral, brain and renal responses, suggesting that this early sodium exposure affects the vulnerability of the organisms to chronic non-communicable diseases mainly caused by changes in sodium intake and the regulatory mechanisms of the angiotensin and vasopressin systems.