Melatonin attenuates renal sympathetic overactivity and reactive oxygen species in the brain in neurogenic hypertension.

Sympathetic overactivation contributes to the pathogenesis of both experimental and human hypertension. We have previously reported that oxidative stress in sympathetic premotor neurons leads to arterial baroreflex dysfunction and increased sympathetic drive to the kidneys in an experimental model of neurogenic hypertension. In this study, we hypothesized that melatonin, a potent antioxidant, may be protective in the brainstem regions involved in the tonic and reflex control of blood pressure (BP) in renovascular hypertensive rats. Neurogenic hypertension was induced by placing a silver clip (gap of 0.2 mm) around the left renal artery, and after 5 weeks of renal clip placement, the rats were treated orally with melatonin (30 mg/kg/day) by gavage for 15 days. At the end of melatonin treatment, we evaluated baseline mean arterial pressure (MAP), renal sympathetic nerve activity (rSNA), and the baroreflex control of heart rate (HR) and rSNA. Reactive oxygen species (ROS) were detected within the brainstem regions by dihydroethidium staining. Melatonin treatment effectively reduced baseline MAP and sympathoexcitation to the ischemic kidney in renovascular hypertensive rats. The baroreflex control of HR and rSNA were improved after melatonin treatment in the hypertensive group. Moreover, there was a preferential decrease in ROS within the rostral ventrolateral medulla (RVLM) and the nucleus of the solitary tract (NTS). Therefore, our study indicates that melatonin is effective in reducing renal sympathetic overactivity associated with decreased ROS in brainstem regions that regulate BP in an experimental model of neurogenic hypertension.

Effect of the addition of glycosaminoglycans on bone and cartilaginous development of broiler chickens.

Locomotion issues in broiler production may decrease performance (carcass yield and traits) and lead to high financial losses. This study evaluates the addition of glucosaminoglycans in broiler diets to minimize the lack of proper bone development and joint weakening. The experiment was conducted using 2,160 broilers randomly distributed in a factorial pattern (3 × 3) using 3 levels of glucosamine sulfate (0, 0.12, and 0.24%) and 3 levels of chondroitin sulfate addition (0, 0.08, and 0.16%). Eight repetitions were used for each treatment, distributed in 72 pens with 30 broilers each. There was a quadratic effect on feed conversion for broilers from 1 to 42 d old (P = 0.0123) for the addition of chondroitin, and better feed conversion was obtained by adding 0.08% of chondroitin. The relative tibia weight, the width of the proximal epiphysis and diaphysis presented a linear increased effect in broilers at 42 d old. An interaction was found between the amount of chondroitin × glucosamine and the number of chondrocytes in the proximal cartilage of the tibia (P = 0.0072). There was a quadratic effect of glucosamine levels (P = 0.0107) in the birds that had received the 0.16% addition of chondroitin, and the presence of 0.18% glucosamine increased the number chondrocytes in the cartilage of broilers. These results provide the first evidence that broilers may benefit from increased dietary chondroitin sulfate. These results indicate that the addition of glucosamine and chondroitin sulfates in broiler feed rations might alleviate leg conditions and decrease financial losses in the broiler industry.