Effects of high fat diet on renal dopaminergic system in the rat: its impact on sodium excretion and blood pressure

CANTÚ SM; LEE BM; DONOSO AS; HOCHT C; TRIDA VA; VAGO R; PUYÓ AM; CHOI MR

Mar del Plata

Congreso; LXIV Reunión Anual de la Sociedad Argentina de Investigación Clínica (SAIC); 2019

Sociedad Argentina de Investigación Clínica

Renal dopaminergic system (RDS) promotes sodium excretion andanti-inflammatory actions. Kidneys are one of the main targets of metabolic syndrome, leading tointracellular lipid accumulation, tubular atrophy, interstitial fibrosis andglomerulosclerosis. However, little is known about the effects of a high fatdiet (HFD) on RDS and its impact in hypertension development.MaleSprague-Dawley rats (body weight of 180-200 gr) were randomized in two groups:control  and HFD during 4, 8, 12 weeks;C: standard diet and tap water to drink, HFD: 50% w/w fat added to controldiet. From week 4, HFD vs. C (H&E stain) showed intracytoplasmaticinclusions in the cortex tubular cells; increased interstitial fibrosis (PicrusSirius red); and podocyte shortness and fusion (transmission electronmicroscopy). FENa, UNa.V and diuresis/min decreased significantly comparing HFDvs. C (*p˂0.01 for each one), GFR showed novariation during the studied periods. Systolic blood pressure (SBP) (mmHg):HFD4: 137±3 vs. C4: 120±2, HFD8: 138±2 vs. C8: 120±2, HFD12: 147±2 vs. C12 115±3; p˂0.01. Triglyceridemia (mg/dl): HFD4: 132±9 vs. C4: 60±8, HFD8: 170±9 vs. C8: 60±6, HFD12:168±14 vs. C12: 58±8; p˂0.01. Insulinemia (ng/ml): HFD8: 4,2±0.5 vs.C8: 1,2±0.1, HFD12: 5,3±0.3 vs. C12: 1.1±0.1; p˂0.01. Glycemia increased from week 8 (p˂0.05) and body weight from week 12 (*p˂0.01).Regarding RDS: Urinary L-Dopa(ng/day/kg): HFD4: 209.6±62.5 vs. C4:22.0±0.9, HFD8: 519,8±33.6 vs. C8:27.2±0.4; p˂0.01. Urinary Dopamine (ng/day/kg): HFD4: 353.0±32.8 vs. C4:7.8±0.6, HFD8: 315.5±60.4 vs. C8: 5.3±1.6, HFD12: 207.7±37.7 vs. C12: 48.7±6.7;p˂0.05.In conclusion, HFD reduced urinary dopamineexcretion while increased L-dopa excretion in association withintracytoplasmatic inclusions in tubular cells and modifications in glomerularultrastructure. Structural alterations might leadto dysfunction of RDS and the subsequent development of hypertension by sodiumretention in this experimental model.