Avaliação dos efeitos renais e vasculares das lectinas das algas Caulerpa cupressoides e Pterocladiela capillacea

Abstract

Macroalgae are found worldwide, playing an important role in maintaining the balance marine and conservation of marine biodiversity. Studies with seaweeds present in the coast of Ceará, such as Caulerpa cupressoides and Pterocladiella capillacea has aroused interest in many biological effects. The Caulerpa cupressoides is a green algae belonging to the family Caulerpaceae and Pterocladiella capillacea is a red seaweed of the family Pterocladiacea. Given the potential of these species and their components such as lectins, as well as a few reports of kidneys toxic effects aimed to study effects of lectins cited algae on renal perfusion model, cytotoxic effects on MDCK cells, effects on Blood Pressure (BP) and Heart Rate(HR). Male Wistar rats weighing between 250 and 300g were used in the experiments. Lectins was utilized in perfusion of isolated kidneys at concentration of 10μg/mL. The effects of lectins were evaluated in Pressure Perfusion (PP), Renal Vascular Resistance (RVR), Urinary Flow (FU), Glomerular Filtration Rate (GFR), Percentage of Tubular Transport of Sodium (% TNa+), Potassium (% TK +) and Chloride (%TCl-). The mesenteric artery assay was realized with the lectin Caulerpa cupressoide- LCc at concentrations of 0.1, 0.3, 1, 3, 10, 30; 60, 100, 200, 300 and 400μg/mL., and the tissue was pre-contracted with phenylephrine (PHE) (0.3μmol and 1μmol). The BP and HR were obtained by cannulation of the carotid artery and registers performed by a data acquisition software. The LCc increased RVR and PP at 90 and 120 min, reduced GFR at 60 minutes and reduced the % TNa+, % TK+ and %TCl- at 60, 90 and 120 minutes. The lectin Pterocladiella capillaceae -LPc reduced the FU at 120 minutes and reduction % TNa+, at 90 and 120 minutes. In the study of cytotoxicity, LCc and LPc did not affect viability of MDCK cells. LCc promoted relaxation in mesenteric artery in concentrations of 100, 200, 300 and 400 µg/mL in tissue pre-contracted with PHE to 1.0 micromol, but did not it in tissue pre-contracted with PHE a 0.3 micromol, in concentrations below to 200 µg/mL. LCc promoted deposition of protein material in the tubule and expansion interstice. The LPc caused deposition protein material in the tubule, without changes at the level of interstice. LCc caused slight reduction in blood pressure at concentrations of 100 and 200μg/mL and did not change the Cardiac Frequency (CF) and LPc caused no changes in CF nor the Heart Rate (HR). It was noted that the LCc promoted renal hemodynamic effects, raising PP and RVR, which may be due to α-adrenoceptor activation. LCc reduced the BP from the concentration of 100 μgmL, suggesting possible release of agents vessel dilators, which also would cause fluid accumulation in the interstice as shown kidney histology. LPc did not change the PP and RVR. The HR and BP were not changed with the LPc, suggesting that it does not promote the release of substances that act directly as a vasoconstrictor.