Effect of an increase in brain serotonin on the osmoregulatory response to a hypo- or hyperosmotic load in Wistar and vasopressin-deficient Brattleboro rats.

Serotonin and its receptor agonists stimulate the release of arginine vasopressin (AVP) into peripheral blood under intraventricular injection. To test the hypothesis that brain serotonin can modulate the development of natural osmoregulatory responses, the effect of an increase in endogenous brain serotonin on the response to an intragastric hypo- or hyperosmotic loading was studied in Wistar and AVP-deficient Brattleboro rats. 5-Hydroxytryptophan (5-HTP), the rate-limiting serotonin biosynthesis precursor known to increase the brain level of serotonin, was injected intraperitoneally (5 mg/100 g body weight).

Hydruric response in Wistar and vasopressin-deficient Brattleboro rats to water load under conditions of increased brain serotonin level.

The hydruric response to water load in Wistar rats and homozygous Brattleboro rats with a hereditary defect in the synthesis of vasopressin was studied under conditions of increased brain serotonin level. Serotonin prevented the reduction in reabsorption of osmotically free water in normal rats, but had no effect in vasopressin-deficient Brattleboro rats. Our results suggest that serotonin stimulates vasopressin secretion and interacts with the vasopressinergic system during the realization of osmotic regulation.

[Osmoregulating reactions following serotonin metabolism inhibition or activation].

Effect of p-chlorphenilalanine and 5-hydroxytriptophan on the urine flow (V), glomerular filtration rate (GFR), free water reabsorption (TCH2O), and sodium fraction excretion (ENa.F%) in Wistar rats loaded with water or 2% sodium chloride solution, was studied. It was found that treatment of rats with inhibitor of serotonin biosynthesis, p-chlorphenilalanine (300 mg/kg, 48 hrs before the experiment) had no effect on the kidney response to the water loading in the experimental rats as compared to the control ones: changes in V, GFR, TCH2O and ENa.

Hypothalamic tryptophan hydroxylase and the hypothalamic-pituitary-adrenocortical response to water deprivation and hydration in vasopressin-deficient and normal rats.

The effects of water deprivation and hydration on plasma corticosterone concentration and the activity of tryptophan hydroxylase (TPH), the rate-limiting enzyme in serotonin (5-HT) biosynthesis, in the hypothalamus of vasopressin- (AVP-) deficient homozygous Brattleboro and normal Wistar rats were studied. In the Wistar rats, water deprivation caused an increase in the TPH activity in the anterior and middle (infundibular) parts of the hypothalamus, while hydration did not affect the activity of the enzyme in the anterior hypothalamus but produced an increase in its middle part. In contrast, in the Brattleboro rats, water deprivation had no effect on TPH activity in the anterior and middle parts of the hypothalamus but hydration produced a decrease in TPH activity in the anterior hypothalamus.

Effects of vasopressin on hyaluronate hydrolase activities and water permeability in the frog urinary bladder.

The involvement of enzymes catabolizing hyaluronic acid (hyaluronidase, beta-glucuronidase, N-acetyl-beta-D-hexosaminidase) in the hydroosmotic effect of vasopressin in the frog (Rana ridibunda) urinary bladder was studied. It was observed that vasopressin (50 nM), an agonist of V2 receptors, L-desamino-8-D-arginine-vasopressin (dDAVP, 1.5 microM) and forskolin (30 microM) activated the enzymes and caused their release into Ringer solution at the mucosal side, together with an increase in osmotic water flow.