Cargando…
Effects of Voluntary Sodium Consumption during the Perinatal Period on Renal Mechanisms, Blood Pressure, and Vasopressin Responses after an Osmotic Challenge in Rats
Cardiovascular control is vulnerable to forced high sodium consumption during the per-inatal period, inducing programming effects, with anatomical and molecular changes at the kidney, brain, and vascular levels that increase basal and induce blood pressure. However, the program- ming effects of the...
Autores principales: | , , , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9860675/ https://www.ncbi.nlm.nih.gov/pubmed/36678125 http://dx.doi.org/10.3390/nu15020254 |
Sumario: | Cardiovascular control is vulnerable to forced high sodium consumption during the per-inatal period, inducing programming effects, with anatomical and molecular changes at the kidney, brain, and vascular levels that increase basal and induce blood pressure. However, the program- ming effects of the natriophilia proper of the perinatal period on blood pressure control have not yet been elucidated. In order to evaluate this, we studied the effect of a sodium overload challenge (SO) on blood pressure response and kidney and brain gene expression in adult offspring exposed to voluntary hypertonic sodium consumption during the perinatal period (PM-NaCl group). Male PM-NaCl rats showed a more sustained increase in blood pressure after SO than controls (PM-Ctrol). They also presented a reduced number of glomeruli, decreased expression of TRPV1, and increased expression of At1a in the kidney cortex. The relative expression of heteronuclear vaso- pressin (AVP hnRNA) and AVP in the supraoptic nucleus was unchanged after SO in PM-NaCl in contrast to the increase observed in PM-Ctrol. The data indicate that the availability of a rich source of sodium during the perinatal period induces a long-term effect modifying renal, cardiovascular, and neuroendocrine responses implicated in the control of hydroelectrolyte homeostasis. |
---|