06. Cardiovascular and Renal Pharmacology 06.001 Renal effects and gender differences in aged Dahl salt sensitive rats. Costa PHS1, Jorge ARC2, Martins ICMT2, Santos CF2, Nascimento NRF2, Monteiro HSA1, Fonteles MC1,2 1 2 UFC – Fisiologia e Farmacologia, ISCB-UECE Introduction: Dahl salt rats are a genetic model of salt sensitivity hypertension that affects the renal and cardiovascular systems. Some studies in Dahl salt sensitive (DS) rats have shown that blood pressure is higher in female than in male at similar ages after menopause. This observation suggests that loss of sex hormones contributes to the development and progression of renal disease. To evaluate possible renal differences of mature DS male and female, in the absence of neural and humoral mechanisms, we have used isolated perfused kidney method. Methods: Isolated kidneys from 18-month-old male (M) and female (F) DS rats weighing 300 to 360g (n=9) were perfused with Krebs-Henseleit solution containing 6g% of bovine serum albumin previously dialyzed for 24 hours and perfused for 120 minutes. The gender differences were studied on glomerular filtration rate (GFR), urinary flow (UF), perfusion pressure (PP), renal vascular resistance (RVR) and percentage of total transport of sodium (%TNa+) and potassium (%TK+) at 30, 60, 90 and 120 minutes of experiment. All data were analyzed by unpaired t test with level of significance of *p pD2 E-: 4.76 ± 0.27, n=6; p ME E-: 22.88 ± 2.70, n=6, p0.05, CR vs. NOQ-UUO-Sal, Student's t-test, P>0.05). UUO increased the picrosirius red-stained areas (%) of renal parenchyma, an alteration that was abolished by CG treatment or OQ; TR reverses the effects of OQ, and CG treatment partially inhibits the effects of hormone replacement (2.19 ± 0.5a, 5.37 ± 0.61b, 2.30 ± 1.06a, 1.95 ± 0.35a, 1.62 ± 0.23a, 5.65 ± 1.33b, 3.90 ± 0.75ab; CR, NOQ-UUO-Sal, NOQ-UUO-CG, OQ-UUO-Sal, OQ-UUO-CG, OQ-UUO-SalTR and OQ-UUO-CG-TR, respectively. Means sharing the same superscript are not significantly different from each other, P>0.05, ANOVA/Newman-Keuls). Conclusion: The data suggest that mast cells and testosterone interact in the development of renal fibrosis induced by UUO. Financial support: This work was supported by a master fellowship by the Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) for Oliveira-Silva, GL. CEUA/UFU: process n° 0132/13.

06.099 Vasorrelaxant effect of R(+)-pulegone in rats. Alustau Fernandes MC1, Mendes-Neto JM2, Santos-Vidal R2, Correia NA3, Albuquerque KLG3, Capettini LAS4, Lauton-Santos S5 1CFPESTC-UFCG, 2PROCFIS-UFS, 3CCS-DFP-UFPB, 4UFMG, 5UFS Introduction: R (+)-pulegone is a monoterpene ketone with blocker properties of calcium channels in the heart. The administration of substances that blocks calcium channels and nitric oxide production stimulates modify the vascular tone of the aorta and trigger reduction of pulsatile pressure, becoming essential for therapy in isolated systolic hypertension, which is the most common disease in the elderly population. Methods/ Results: vasorrelaxant effects of R (+)-pulegone were tested in normotensive rats using two different methodological approaches. In vivo, increasing doses (1, 3, 10, 20 and 30 mg / kg) were administered in the animals, i.v. bolus and selected randomly, then the parameters for mean arterial pressure (MAP) and heart rate (HR) were evaluated. In this situation the substance triggered a hypotensive effect and bradycardia. In the ex vivo approach, we used the thoracic aorta of these animals and isometric tension experiments, evaluated the vasorelaxant activity of the substance. The administration of R(+)-pulegone triggered vasorelaxant effect concentration-dependent in both rings with intact endothelium and with this removed, but the substance had the lowest pD2 value in the presence of the endothelium (-3.64 ± 0.06, n = -3.17 vs 5 ± 0.034, n = 6, respectively), no change in peak effect (98.2 ± 1.2%, n = 5 vs. 106.0 ± 8.1%, n = 6) indicating that the substance acts triggering vasodilation in aortic dependent manner and independent of the vascular endothelium. In rings with intact endothelium, the vasorelaxant activity of R (+) - pulegone was not altered in the presence of diclofenac and atropine, but was modified by L-NAME (-3.00 ± 0.016; n=5), HDX (hydroxocobalamin) (-3.07 ± 0.021; n=5), ODQ () (-3.17 ± 0.03; n = 5) and the red ruthenium (-3.14 ± 0.04; n=5) vs control: -3.64 ± 0.06; n = 5. These results suggest that the substance is probably stimulating NO production via the activation of TRP (transient receptor potential) channels. In smooth muscle vascular, R (+)-pulegone inhibited curve calcium concentration-dependent manner (Emax: 10-4 M: 68 9 ± 3.81%; 3x10-4 M: 40.97 ± 8.05%; 10-3 M: 24.79 ± 5.04% and 3x10-3 M: 0.29 ± 0.33%) via calcium channels type L, as in the presence of nifedipine, there was a reduction of the maximum effect (Emax: 93.3 ± 1.7% ; n = 6 vs Emax control: 106.8 ± 8.1%; n = 6 ). Additionally, it was surveyed the participation of for potassium channels, using 4-aminopyridine (-2.93 ± 0.012 - n = 5 vs control - 3.17 ± 0.034 - n = 6), since, in the presence of glybenclamide, the relaxant response to R (+)-pulegone was also inhibited (2.94 vs. -3.17 ± 0.012 ± 0.03).Conclusion R (+)-pulegone, stimulates the production of NO (nitric oxide) in endothelial cells, probably by activating calcium influx via TRP channels. The effect independent of the endothelium is mediated by inhibition of calcium influx, likely through the CaVs and for opening potassium channels (KATP and Kv). Financial Support: CNPq Animal Research Ethical Committee: All approaches of this study was approved by CEPA/UFS (nº #4/2015)