The role of the antidiuretic hormone during water deprivation in rats

Abstract

It has been suggested that the survival of animals deprived of water is in direct proportion to their ability to concentrate their urine, and that the high concentration of their urine is achieved at the expense of an increased secretion of the antidiuretic hormone. The problem investigated here was to see whether the decrease of the urinary volume observed in laboratory rats deprived of water was the sole factor in the mechanism of water preservation and if so, whether the reduction of urinary secretion was the result of a corresponding increase in secretion of the antidiuretic hormone. METHODSWhite adult male rats of body weight ranging from 250 to 325 g were fed on a standard diet, 100 g of which contained: protein 14 g, fat 4 g, and soluble carbohydrate 49 g; calorific yield 400 call 100 g. From its composition, it could be calculated that its metabolic water was 52 ml./100 g food: its amount of moisture (i.e. 'preformed water') was 13-0 ml./100 g. The water content of food and of faeces was estimated by drying in an oven at 1040 C for 48 hr. The rats were kept in metabolism cages, at a temperature of 210 C; the degree of humidity was not recorded. Urine separators were fixed to the cages and the faeces were collected separately in a vessel with narrow neck so as to diminish water evaporation. Whenever possible fresh faeces were collected for the estimation of their water content. For the estimation of its antidiuretic activity urine was collected in a solution of 3 % (v/v) acetic acid (final concentration, 0-2-0-3 %). Pituitary glands were removed, dried and extracted as specified in the British Pharmacopoeia (1953); the amount of acetic acid used in their extraction did not exceed 0-2 ml./gland of a 0-25 % acetic solution (Bentley & Dicker, 1955). Urine samples were analysed for their Na and K content, using an EEL flame photometer; occasional Cl estimations were performed.The antidiuretic activity of urine or of dissected neurohypophyseal glands was estimated by intravenous injection in rats under ethanol anaesthesia, with the water load kept constant (Dicker, 1953). The vasopressor activity of the neurohypophysis was estimated on rats anaesthetized with urethane and injected with dibenamine (Dekansky, 1952) and the oxytocic activity on a rat's isolated uterus (Holton, 1948). Each assay of the antidiuretic, vasopressor or oxytocic activity consisted of four doses, two of the standard and two of the unknown, the ratio, high to low dose, being the same for standard and unknown solutions. Results were expressed in terms of the antidiuretic or vasopressor activity of a solution of vasopressin, or in terms of oxytocic activity of a solution of oxytocin.

Fate and excretion of the pressor activity of vasopressin in rats

“…The errors of the method fell within the limits stated previously (Dicker & Nunn, 1957). Nephrectomy and evisceration were performed on rats under ethanol anaesthesia, induced by the administration of 5 ml./100 g of a 12% (v/v) ethanol solution, and maintained, if necessary, by intravenous injections of 1 ml.…”

“…In four similar experiments the mean pressor activity of the urine of the second 'recipient' eviscerated rats was 4-7 + 0-82 % of the urinary pressor activity infused (Table 3). As the injection of urine does not affect the excretion of vasopressin simultaneously administered (Dicker & Nunn, 1957), these results suggested that the 'recipient' eviscerated rat dealt with the pressor activity of the urine from the eviscerated 'donor' in the same way as the latter had done with infused vasopressin. This was also suggested by the following experiment: four eviscerated rats were each infused with 1000 m-u.…”

The effect of vasopressin (Pitressin) administration and dehydration on the concentration of solutes in renal fluids of rats with and without hereditary hypothalamic diabetes insipidus

“…2), when maximum osmolality reached was 4560 with a mean of 3300 m-osmole/kg. The dehydration was not continued for a longer period as it has been shown (Dicker & Nunn, 1957) that the maximum urine osmolality is achieved 72 hr after water withdrawal.…”

“…The latter has been shown to raise the concentration of the urine, even in the absence of vasopressin, in the dog (del Greco & de Wardener, 1956;Berliner & Davidson, 1957) and in the rat (Dicker, 1957). However, vasopressin administration alone will not increase the urinary concentration to the same extent as that found with dehydration in man (West, Traeger & Kaplan, 1955;Jones & de Wardener, 1956;Epstein, Kleeman & Hendrikx, 1957), dog (West et al 1955) or rat (Dicker & Nunn, 1957). Recently, Atherton et al (1971 a) have demonstrated that hydropenia combined with vasopressin resulted in a somewhat higher sodium concentration than vasopressin infusion alone in the medulla of the conscious Wistar rat.…”

THE HYPOTHALAMO‐NEUROHYPOPHYSIAL SYSTEM OF NATIVE AUSTRALIAN DESERT RODENTS. THE VASOPRESSIN AND OXYTOCIN CONTENTS OF HYPOTHALAMUS AND POSTERIOR PITUITARY OF NOTOMYS ALEXIS AND PSEUDOMYS AUSTRALIS COMPARED WITH THOSE OF THE LABORATORY RAT AND MOUSE IN DIFFERENT STATES OF WATER BALANCE

“…Rats subjected to 8 days of saline imbibition reacted similarly to those on dry diet and the change.s observed in both groups were not significantly different from those of the water deprivation studies on the rat by Dicker and Nunn (1957); Jones and Pickering (1969);Bridges (1970) ;Castel and Abraham (1972) and Guzek. Orlowska-Majdak and Wdzieczak (1976).…”