The Effect on Vasopressin Release of Microinjection of Cholinergic Agonists into the Paraventricular Nucleus of Conscious Rats

Abstract

We have studied in conscious unrestrained rats under basal conditions the effect of activation of muscarinic and nicotinic receptors in the paraventricular nucleus on vasopressin secretion and mean arterial blood pressure. The microinjection of oxotrernorine (0.2, 2 or 20 ng), a specific muscarinic agonist, produced a substantial, dose-dependent, transient increase in the plasma vasopressin concentration. There was also a rise in mean arterial blood pressure and a bradycardia that followed the same time-course as the change in plasma vasopressin levels. The microinjection of nicotine (0.1, 1 or 10 pg) into the paraventricular nucleus had only questionable effects on vasopressin release and mean arterial blood pressure; heart rate was unaffected. These findings suggest that muscarinic receptors may be of primary importance in the paraventricular nucleus in the cholinergic stimulation of vasopressin re I ease.There is considerable evidence to suggest that central cholinergic mechanisms play a n important role in the control of vasopressin release. It has been reported that cholinergic neurons project to the paraventricular (PVN) and supraoptic nuclei (SON) (1-3). Acetylcholine and its synthetic and degradative enzymes, i.e. clioline acetyltransferase and acetylcholine esterase, have been demonstrated in the anterior hypothalamus and posterior pituitary (4-7). Receptors for acetylcholine have been demonstrated in the PVN, . Finally, the central administration of acetylcholine and its agonists (18-23) in the intact animal, and the addition of acetylcholine to the medium in which the isolated hypothalamo-neurohypophysial complex is incubated (24, 25), stimulate the release of vasopressin.It is, however, controversial whether the cholinergic receptors involved in the stimulation of vasopressin release are muscarinic 01 nicotinic. Recently, Iitake et at. (23) found that the intracerebroventricular (icv) administration of carbachol stimulated the release of vasopressin in the conscious rat and that this effect was blocked by atropine, but not by hexamethonium, suggesting that the receptors are muscarinic. These observations are in agreement with those of earlier studies in the rat (20,26), dog (18), goat (19), and sheep (22), in which antidiuresis was used as an index of vasopressin release. On the other hand, there is also evidence that activation of nicotinic receptors in the SON elicits the release of vasopressin in the rat (24, 25, 27) and cat (21, 28).In an effort to resolve the issue of the nature of the cholinergic receptors in the PVN, we have, in the present study, determined the effect on vasopressin release of the microinjection of muscarinic and nicotinic agonists into the PVN. ResultsThe microinjection of the artificial cerebrospinal fluid (aCSF) vehicle into the PVN and the taking of blood samples were without effect on the plasma vasopressin concentration (Fig. I), mean arterial blood pressure (Fig. 2), heart rate ( Fig. 2), plasma osmolality and hematocrit. However, the microinjection of oxotremo...

The effect of neosurugatoxin on the release of neurohypophysial hormones by nicotine, hypotension and an osmotic stimulus in the rat

“…Agonists acting on muscarinic cholinoceptors have been shown to release vasopressin and oxytocin in the rat and this release is blocked by atropine (Kuhn & McCann, 1971;Kuhn, 1974;Clarke & Merrick, 1978;Bisset & Chowdrey, 1984;litake et al, 1986;Shoji et al, 1989). In our experiments, NSTX acted selectively on nicotinic, and not on muscarinic, receptors.…”

Release of vasopressin and oxytocin by excitatory amino acid agonists and the effect of antagonists on release by muscarine and hypertonic saline, in the rat in vivo

“…The response was blocked by EAA antagonists (Gribkoff & Dudek, 1990;Gribkoff, 1991). Recently it has been shown that oxotremorine, an agonist acting selectively on muscarinic cholinoceptors, induces an ADR on microinjection into the SON or PVN (Mori et al, 1984) or release of AVP into the circulation on injection into the PVN but not the SON; nicotine caused release on injection into the SON (Shoji et al, 1989;Ota et al, 1992 CNQX are consistent with differences in the anatomy of the cholinergic and noradrenergic innervation of the SON and PVN. The noradrenergic input is derived mainly from the Al group of neurones in the ventrolateral medulla (Sawchenko & Swanson, 1981).…”

A-type K+ channels contribute to the prorenin increase of firing activity in hypothalamic vasopressin neurosecretory neurons

“…Although the roles of the peripheral RAS are well established, there is still an ongoing debate related to the contribution and mechanisms by which the central RAS influences cardiovascular control (43,52). For example, all RAS components are expressed in the SON and PVN (29), as well as ANG II and AT 1 Rs, have been proposed as key players underlying RAS-mediated increases in sympathoexcitatory outflow and VP systemic release (24,35,42,53). However, recent studies have provided evidence for the lack of AT 1 Rs and ANG II type 2 receptors on presympathetic and VP cells (9 -11), whereas others have supported the contribution of astroglial cells as alternative cellular targets mediating central ANG II actions in these neuronal populations (3,49).…”

“…it is now well accepted that all components of the RAS are also present within the central nervous system, which, acting independently of the peripheral RAS, can directly influence autonomic and neuroendocrine outflows to the cardiovascular system (8,16). For example, activation of the brain RAS, involving predominantly ANG II and ANG II type 1 receptors (AT 1 Rs), increases sympathoexcitatory outflow and vasopressin (VP) systemic release (24,35,42,53). Despite this evidence, there is still an ongoing debate regarding the localization, sources, cellular targets, and roles of the main RAS components within the brain.…”