El losartan previene la alteración en la liberación de prostanoides vasculares producida por una dieta alta en grasa en la rata

LEE HJ; CANTÚ SM; ALVAREZ PRIMO M; DONOSO AS; CHOI MR; PEREDO H; PUYÓ AM

Ciudad Autónoma de Buenos Aires

Congreso; XXV Congreso Argentino de Hipertensión Arterial (SAHA); 2018

Sociedad Argentina de Hipertensión Arterial (SAHA)

Metabolic diseases are linked to hypertension. High-fat (HF)diet in rats is an experimental model that resemble the human metabolicsyndrome. The mechanisms that trigger the blood pressure (BP) increase in thismodel are not fully understood. Prostanoids (PR) play an important role invasomotor tone regulation. The aim of this study was to analyze metformin (M)and losartan (L) effects on mesenteric vascular bed (MVB) PR release, adiposityindex and its relation to BP. Six groups (n=6) of male Sprague-Dawley rats werestudied during 8 weeks: Control (C), standard diet (SD) and tap water (W) todrink; HF diet (HF), 50% (w/w) bovine fat added to SD and W; C + M (CM), SD +500 mg/Kg/day M in W to drink; C + L (CL), SD + 30 mg/Kg/day L in W to drink;HF + M (HFM) 500 mg/Kg/day M in W to drink; HF + L (HFL) 30 mg/Kg/day L in W todrink. MVBs were removed and incubated and the released PRs measured by HPLC.HF diet increased systolic BP (SBP, mmHg, HF: 145±5 vs. C: 118±2, p<0.01);MVB adiposity index (%, HF: 1.7±0.1 vs C: 0.9±0.04, p<0.01); and the releaseof vasoconstrictor PR such as thromboxane (TX) B2 (ng PR/mg of tissue, HF:117±6 vs C: 66±2, p<0.001) and prostaglandin (PG) F2α (ng/mg, HF: 153±9 vs C: 88±3,p<0.001). In HFM and HFL groups, M and L treatment prevented the increasesof SBP (HFM: 127±2, HFL: 111±3 vs. HF, p<0.001 and p<0.01), TXB2 release(ng PR/mg of tissue, HFM: 65±12, HFL: 66±7 vs. HF, p<0.05 and p<0.01);and PGF2alpha (ng PR/mg of tissue, HFM: 99±13, HFL: 90±7 vs. HF, p<0.01 andp<0.05). Meanwhile M also prevented the increase of MVB adiposity index (%,HFM: 1.3±0.2 vs HF, p<0.05). Treatments with M and L could exert beneficialeffects on the vascular system improving endothelial dysfunction by preventingthe increase of vasoconstrictor PR in MVB. In addition, M prevents adiposity increase.