Participation of the median raphe nucleus and central serotoninergic pathways in the control of water electrolyte excretion

RESUMO

1. The role of the median raphe nucleus (MRN) and of increased central serotonin (5HT) synthesis/release in the mediation of Na+ excretion (UNaV) and K+ excretion (UKV) and or urine output (UV) was evaluated for 120 min. 2. Male Wistar rats weighing 220-280g were used in each group of 12-13 animals. The rats implanted with a cannula in the MRN were injected with saline (0.5 µl) or with 5.0 and 15.0 ng/0.5 µl kainic acid (KA), an excitatory amino (EAA). Another group of rats was injected ip with 200 mg/Kg saline or tryptophan, the initial precursor of 5HT synthesis. 3. Injection of both kainic acid and tryptophan led to increased Na+ excretion, but the magnitude and time course were different for each treatment. Both KA doses were effective in increasing UNaV (0.061 ñ 0.08, mean ñ SEM, and 0.95 ñ 0.19 -Eq/min, respectively, vs 0.27 ñ 0.04 µEq/min for saline at 60 min). The effect on UKV was statistically significant with the 15.0 ng dose (0.44 ñ 0.05 µEq/min vs 0.25 ñ0.03 µEq/min for saline) at 20 min. 5. Tryptophan adminsitration caused an initial gradual increase in UNaV which became steady and significant after 60 min (1.02 ñ 0.15 µEq/min vs 0.36 ñ 0.06 µEq/min for saline), as well as an increase in UKV (0.58 ñ 0.06 µEq/min vs 0.26 ñ 0.04 µEq/min for saline) at 60 min and throught the remainder of the observation period. 6. KA-induced MRN stimulation and systemic tryptophan overload significantly increased UV at 60, 80 and 100 min (30 to 97% above control values). 7. These data show that kanic acid-mediated transmission at the MRN lellvel may play a modulatory role in hydromineral metabolism. The effects obtained after increased central availability of tryptophan suggest that the excretory response is associated with an increase in 5HT synthesis/release and with an increase in central transmission. 8. We conclude that the data obtained from CA-induced MRN stimulation and systemic tryptophan overload may possibly reflect an increased 5HT synaptic transmission at sites and efferent mechanisms that remain to be elucidated