ABSTRACT
Objectives: Metabolic syndrome is associated with the development of chronic kidney disease. Bursera simaruba "chaca" is a medicinal plant used in Mexico for hypertension and empirical therapy. In this study, were examined the effects of ethanol extract of B. simaruba on metabolic syndrome. Materials and Methods: For induction of metabolic syndrome, 20% fructose was used, and it was administered in the water and food to male Wistar rats for 12 weeks, after administering ethanol extract of B. simaruba intragastrically (100 and 200 mg/kg/day) for 6 weeks, blood pressure was determined. In plasma, glucose, cholesterol, triglycerides, angiotensin II, oxide nitric, and angiotensin 1-7 were quantified. In the kidney was performed histological study and the activity of anti-oxidant enzymes was quantified. Results: Rats with metabolic syndrome developed obesity, arterial hypertension, dyslipidemia, and kidney damage characterized by proliferative glomerulonephritis, necrosis, and reduced activity of anti-oxidant enzymes. These alterations were significantly ameliorated by ethanol extract of B. simaruba. Conclusion: The ethanolic extract of B. simaruba showed antidyslipidemic, antihypertensive, anti-oxidant, and renoprotective effects.
ABSTRACT
Shear stress stimulates nitric oxide (NO) release in endothelial cells. Stretch-activated ion channels (SACs) and the transient receptor potential vanilloid type 1 (TRPV1) receptor respond to mechanical stimulus and are permeable to Na(+), Ca(2+) and K(+). The influence of SACs and the TRPV1 receptor on NO release on the heart and on the vascular reactivity of the thoracic aorta (TA) was studied. Experiments were performed in isolated perfused heart, cultured endothelial cells and TA rings from Wistar rats. Capsaicin (10 µM, 30 µM) was used as a NO release stimulator, capsazepine (6 µM, 10 µM) was used as a capsaicin antagonist and gadolinium (3 µM, 5 µM) was used as an inhibitor of SACs. NO was measured by the Kelm and Tenorio methods. Left ventricular pressure was recorded and coronary vascular resistance was calculated. Capsaicin increased NO release in the heart by 58% (395±8 pmol/mL to 627±23 pmol/mL). Capsazepine and gadolinium inhibited NO release by 74% and 82%, respectively. This tendency was similar in all experimental models. Capsaicin attenuated the effects of norepinephrine (10 M to 7 M) on TA and had no effect in the presence of N (ω)-nitro-L-arginine methyl ester. Therefore, the authors conclude that SACs and the TRPV1 receptor are both present in the coronary endothelium and that both participate in Ca(2+)-dependent NO release.
ABSTRACT
The convenience to count with a safe and effective pharmacological wealth for atrial fibrillation treatment had conduced, in a way, to a deep depuration of the vast array of antiarrhythmic drugs, keeping only a very restricted number of compounds with a widely proved anti-atrial activity. On the other hand, it had lead to the discovery of the pathophysiological concepts that point to novel therapeutic targets. Within these objectives is that new antiarrhythmic drugs with preferential, even selective, activity on myocardial atrium ion channels had been developed. Among these new antiarrhythmics, dofetilide, and AVE0118, are taken into account. In addition, new possibilities are opened based on the knowledge of the cardioprotective-antiarrhythmic qualities of the opioidergic system.
