Inhibitory effect of galanin on dopamine-induced enhanced vasopressin secretion in rat neurohypophyseal tissue cultures.

The effect of galanin (GAL) on vasopressin (VP) secretion was studied in 13-14-day cultures of isolated rat neurohypophyseal (NH) tissue. The VP content of the supernatant was determined by radioimmunoassay (RIA) after a 1- or 2-h incubation. A significantly decreased content of VP was detected following the administration of 10(-6)-10(-9) M doses of GAL. Dopamine (DA) and the DA-active drugs apomorphine (APM) and Pro-Lys-Gly (PLG) (10(-6) M in each medium) increased the VP level of NH tissue cultures. This VP concentration elevation could be blocked by the administration of GAL together with DA, APM or PLG. The DA-blocking effect of GAL was prevented by previous treatment with the GAL receptor antagonist galantid (M15). The results indicate that VP release is directly influenced by the GAL-ergic system. The GAL-ergic control of VP secretion from NH tissue in rats can occur independently of the hypothalamus, at the level of the posterior pituitary.

Vasopressin pressor receptor-mediated activation of HPA axis by acute ethanol stress in rats.

The plasma arginine vasopressin (AVP), ACTH, and corticosterone levels and the hypothalamic corticotropin-releasing hormone (CRH) content were measured after oral administration of 1 ml of 75% ethanol to rats, a model known to induce acute gastric erosions and stress. Elevated plasma AVP, ACTH, and corticosterone levels were detected 1 h after ethanol administration. Treatment with the vasopressin pressor (V(1)) receptor antagonist [d(CH(2))(5)Tyr(Me)-AVP] before ethanol administration significantly reduced the ACTH and corticosterone level increases. A higher hypothalamic CRH content was measured at 30 or 60 min after ethanol administration. V(1) receptor antagonist injection, 5 min before ethanol administration, inhibited the rise in hypothalamic CRH content. The protein synthesis blocker cycloheximide prevented the hypothalamic CRH content elevation after stress. The AVP-, CRH-, and AVP + CRH-induced in vitro ACTH release in normal anterior pituitary tissue cultures was also prevented by pretreatment with the V(1) receptor antagonist. The results support the hypothesis that stress-induced AVP may not only act directly on the ACTH producing anterior pituitary cells but also indirectly at the hypothalamic level via the synthesis and release of CRH.

Immunoelectronhistochemical evidence for innervation of brain microvessels by vasopressin-immunoreactive neurons in the rat.

Peroxidase-antiperoxidase (PAP) immunocytochemistry at the electron microscopic level was used to describe the fine structural characteristics of vascular connections between vasopressin (VP)-immunoreactive neuronal elements and cerebral microvessels in the rat. In the majority of connections, somata or neural processes (mainly dendrites) showing VP-like immunoreactivity were separated from the vessel wall by thin glial processes. In addition, some VP-positive elements could establish direct contacts with the basal lamina of the endothelium or of a pericyte associated with the capillary bed. The findings provide immunocytochemical evidence that the vasopressinergic neuronal elements can directly innervate microvessels in the brain and thereby participate in regulating the local permeability of and the flow through the cerebral microvessels.

Hereditary diabetes insipidus in rats. Altered cerebral indolamine and catecholamine metabolism.

Compared to heterozygous Brattleboro animals, homozygous (diabetes insipidus) rats exhibited higher steady-state levels of serotonin in the mesencephalon, septum and striatum. These differences disappeared upon the administration of pargyline, suggesting accumulation of serotonin. The norepinephrine level was higher in the mesencephalon, while the disappearance rate (alpha-met hyl-p-tyrosine) was accelerated in the septum and decreased in the hypothalamus. The lower striatal dopamine level was associated with a decreased disappearance rate. The data suggest that the altered monoamine metabolism might be associated with the known endocrine and behavioral disturbances of the homozygous rats.

The ADH-reserve capacity in Brattleboro rats.

The water metabolism was studied in homo- and heterozygous Brattleboro rats suffering from hereditary hypothalamic diabetes insipidus. In homozygous Brattleboro rats the spontaneous water intake and urinary output and the diuretic reactions signficantly increased after water and salt loading. No antidiuretic activity was found in the urine, posterior pituitary or hypothalamus of these animals, and this state was not affected by hyperosmosis. For the heterozygous rats the spontaneous water intake and urinary output and the diuretic reaction exceed the respective control values, the posterior pituitary, the hypothalamus and the urine are of reduced antidiuretic activity and this activity is less mobilizable by hyperosmosis. It is concluded that the ADH-reserve deficiency is total in the homozygous Brattleboro rats, and partial in the heterozygotes. As a result of hyperosmosis, the vasopressin release is of a reduced extent, yet detectable in the heterozygotes.