Interaction of changes in the third ventricular CSF tonicity, central and systemic AVP concentrations and water intake

Abstract

Arginine vasopressin (AVP) is assumed to be involved as a central transmitter or modulator in the control of autonomic functions including thirst. In conscious dogs AVP concentration in cerebrospinal fluid (CSF) from the anterior part of the third ventricle (A3V) was analysed before and after local elevation of CSF osmolality by intracerebroventricular (i.c.v.) infusion of 0.35 M NaCl and after i.c.v. AVP infusion at 46 and 138 fmol ml-1 for 10 min. In addition, the effects of these i.c.v. infusions on water intake, plasma AVP concentration and blood pressure were investigated. In euhydrated dogs 0.35 M NaCl i.c.v. did not alter AVP concentration in the CSF during the subsequent 2 h. In contrast, plasma AVP concentration had increased significantly from 3.4 +/- 0.3 (control) to 6.4 +/- 0.7 and 4.7 +/- 0.3 fmol ml-1, 4 and 16 min, respectively, after the hypertonic stimulus. Drinking was stimulated with an average water intake of 14.5 +/- 3.7 ml kg-1 body wt. However, AVP infusion into the A3V did not elicit water intake despite increases of AVP concentration in the A3V by factors up to 40 above control. The same animals responded with spontaneous drinking to 0.35 M NaCl i.c.v. administered 160 min after the end of AVP infusions. Exogenously administered AVP disappeared from the A3V with a time constant of 13.8 min. The results do not support the view that AVP in the A3V CSF per se stimulates drinking.

Excitatory action of the bird antidiuretic hormone vasotocin on neurons in the subfornical organ

“…In constrast to a previous study by the same authors, the AVP concentration in the SFO is not increased but remains stable after 1 3 days of water withdrawal (Summy-Long et al 1978. Similarly uncertain is the effect of centrally and peripherally applied AVP on water intake, because facilitatory (Szczepanska-Sadowska et al 1982), inhibitory (on drinking induced by water deprivation, Rolls 1971) and no effects on drinking have been described in both rat and dog (Eriksson et al 1987;Rolls 1971), while this parameter has not been investigated for AVT in a bird species so far.…”

“…AVP applied into the 3rd ventricle of dogs even at 40 times higher concentration (1200 fmol/ml) than the basal concentrations (30 fmol/ml) in the cerebrospinal fluid did not induce drinking in this species, thus speaking against a role of central, hypothalamic ADH on water intake (Eriksson et al 1987). This conclusion, however, does not take into account that icy.…”

“…Intravenously applied AVP had either no effect on water intake in rats, or inhibited NaC1 induced drinking (Rolls 1971). Only a single study exists in which ADH injection into the third ventricle produced dipsogenic effects in dogs (Szcepanska-Sadowska et al 1982), but this effect could not be reproduced in subsequent studies on the same species (Eriksson et al 1987). The failure to observe a relevant osmoregulatory effect of ADH on the best characterized SFO mediated function, namely drinking, is presumably the reason, why the receptive function of SFO neurons for circulating or locally released ADH has not been investigated on the cellular level so far.…”

Involvement of non-neuronal brain cells in AVP-mediated regulation of water space at the cellular, organ, and whole-body level

“…In vivo, choroidal AVP is likely to be released to ventricular CSF Lipinska and Buijs, 1988). The CSF concentration of AVP is 20 -30 pg/ml or 3 ϫ 10 Ϫ11 M, which is several times higher than the plasma concentration (Simon-Oppermann et al, 1983;Eriksson et al, 1987;Lipinska and Buijs, 1988;van Esseveldt et al, 1999). It is possible that choroidal release of AVP may lead to sufficiently high local levels to alter CSF formation.…”

Systemic salt loading decreases body temperature and increases heat‐escape/cold‐seeking behaviour via the central AT1 and V1 receptors in rats

“…An increase in plasma osmolality during dehydration and/or salt loading elevates angiotensin II (AII) and arginine vasopressin (AVP) concentrations in both the plasma and cerebrospinal fluid (CSF; Thrasher et al 1980; Simon‐Oppermann et al 1983, 1986; Szczepanska‐Sadowska et al 1983, 1984 a , b ; Doris & Bell, 1984; Eriksson et al 1987; Jolkkonen et al 1988). These two hormones have binding sites throughout the brain, and AT 1 receptors for AII and V 1 receptors for AVP are abundant (Phillips et al 1988; Gerstberger & Fahrenholz, 1989; McKinley et al 1990).…”