Antidiuresis of Centrally Administered Amines and Peptides and Release of Antidiuretic Hormone from Isolated Rat Neurohypophysis

Abstract

Abstract-Effectsof biogenic amines and peptides on urine outflow and ADH release were studied using intracerebroventricular (i.c.v.) perfusion experiments and isolated neurohypophysis incubation studies. Decrease in the urine outflow was observed after norepinephrine, histamine and angiotensin II had been administered i.c.v.. The effect of norepinephrine was prevented by phentolamine.Phentolamine alone also acted as an antidiuretic.a-Adrenergic and histaminergic mechanisms may thus involved in ADH releasing system and this system might be also responsive to angioten sin II. When the isolated neurohypophysis was incubated in the presence of nore pinephrine, histamine, angiotensin II amide 5-valine or bradykinin, release of ADH was increased, and the effects of norepinephrine and histamine were prevented by phentolamine and promethazine, respectively.Phentolamine but not promethazine alone increased ADH release. On the other hand, serotonin, dopamine and angio tensin II 5-isoleucine did not result in an ADH release from the isolated neural lobes. Our findings suggest that when the local concentration of norepinephrine, histamine or peptides is increased to the extent where the posterior lobe of the pituitary is stimu lated directly, the ADH release is enhanced.Norepinephrine (also probably dopamine)-containing nerve terminals have been found in the supraoptic nucleus (SON) and paraventricular nucleus (PVN) of the hypothalamus (1). Antidiuretic hormone (ADH) produced in the nerve cells in the SON and PVN is transported to the posterior lobe of the pituitary. It seems likely, therefore, that an adre nergic mechanism is implicated in the production and secretion of ADH. In fact, centrally administered norepinephrine stimulated the release of ADH (2-4). Although relatively high concentrations of histamine (5-7) and angiotensin (8) are found in the brain, particularly in the hypothalamus, little is known about their role in the mechanisms of ADH release.The present experiments dealt with possible roles of these biogenic amines and the peptides on the central antidiuresis using an intracerebroventricular (i.c.v.) perfusion technique in rats.Whether or not biogenic amines and peptides stimulate directly the release of ADH from the isolated neurohypophysis was also studied. It has earlier been shown that angio tensin II increases the ADH release from the isolated neurohypophysis (9), and it was sug gested that the antidiuretic effect of bradykinin was due to its action on the central nervous system, although bradykinin did not cause a release of ADH from the isolated preparation (10). Furthermore, there is no data which suggests that the amines stimulated directly the neurohypophysis to increase the ADH release.

EFFECTS OF INTRACEREBROVENTRICULAR PROSTAGLANDINS E2 AND F2α ON THE URINE OUTFLOW, AND a POSSIBLE ROLE OF PGE2 AS a MODULATOR

“…Both antidiuretic and ADH releasing effects of noradrenaline were inhibited by phentolamine (15,20,21). This may be an a-adrenergic effect, as speculated by others (21).…”

“…Noradrenaline, when injected centrally, was an antidiuretic (15,19,20) and caused an increase in plasma ADH concentration (20,21). Both antidiuretic and ADH releasing effects of noradrenaline were inhibited by phentolamine (15,20,21).…”

THE EFFECT OF PROSTAGLANDIN E2 MICROINJECTED INTO THE RAT HYPOTHALAMUS ON URINARY EXCRETION OF WATER AND SODIUM

“…In addition, Hisada et al (1977) found that antidiuresis in response to i.c.v. injected noradrenaline was inhibited by phentolamine but not propranolol.…”

THE HYPOTHALAMO‐NEUROHYPOPHYSIAL SYSTEM OF NATIVE AUSTRALIAN DESERT RODENTS. THE CATECHOLAMINE CONTENTS OF THE HYPOTHALAMUS AND POSTERIOR PITUITARY OF NOTOMYS ALEXIS, PSEUDOMYS AUSTRALIS AND THE LABORATORY RAT

“…Bridges et al, (1976) found that, in addition to its effect in vivo, dopamine in extremely low (femtogram) concentration provoked the release of vasopressin and oxytocin from the rat hypothalamus in vitro and, in much higher (nanogram) concentration, from the isolated neural lobe. Conversely, Johnston et al, (1975) found that dopamine inhibited the electrically-stimulated release of lysine vasopressin from the pig neural lobe in vitro whereas Yeo, Lockett and Heller (1972) and Hisada et al (1977) found that microgram quantities of dopamine did not alter hormone release from the rat neural lobe. Ruoff, Gosbee and Lederis (1974) applied nanogram doses of dopamine directly to the neural lobe of the anaesthetized rat by microinfusion via the transauricular route but could find no change in urine flow or conductivity.…”