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Antidiuretic hormone (ADH) does not always exert its well-known water-retaining action on the kidney (Kleeman, 1972). We have recently demonstrated in sheep that a high salt intake (Burstyn, Horrobin & Manku, 1972) and cortisol treatment (Horrobin, Manku & Burstyn, 1973) can convert the usual sodium-retaining action of aldosterone into a sodium-losing one. Both prolactin and oxytocin can convert aldosterone back into a sodium-retaining substance. We have therefore investigated the possibility that cortisol, prolactin and oxytocin may have interactions with ADH similar to those that they have with aldosterone.
Seven anoestrous Merino ewes were prepared and treated throughout the experiment with a supplement of 80 mequiv. NaCl/day, and urine collections were made as previously described (Burstyn et al. 1972). Each day at 14.00 h an injection of either 15 mu. arginine-vasopressin (Ferring) or of 1 ml isotonic saline was given to each animal through a jugular venous cannula. Preliminary tests had
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SUMMARY
The effects of aldosterone on sodium, potassium and water excretion during various treatment regimes were studied in six Merino ewes. Urine was collected from 12.00 to 14.00 h and from 14.00 to 16.00 h each day. Intravenous injections of either 1 ml isotonic saline or 500 μg aldosterone were given at 13.30 h and excretion during the second collection period compared with that in the first. When each animal was given a salt (NaCl) supplement of 80 mequiv./day by i.v. injection, aldosterone caused marked sodium retention with no effect on potassium. When salt supplements of 400 mequiv./day were given, aldosterone lost its sodium-retaining action in all animals and caused a marked saluresis with a small increase in potassium excretion in five sheep out of six. Injections of sheep pituitary prolactin or of oxytocin restored the sodium-retaining action of aldosterone in spite of a continued high salt intake. The animals gained very little weight when treated with 400 mequiv. salt alone but did gain significantly when treated with salt plus prolactin. The weight gain was rapidly lost when the prolactin and high salt intake were discontinued.
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SUMMARY
Thirty-nine decerebrate rabbits, curarized and maintained by artificial ventilation, were used in the experiments. In a control group which received only saline intravenous infusions, arterial pressure remained virtually unchanged for 6 h after decerebration. Three other groups were used, all of which received intravenous infusions of aldosterone starting 1 h after decerebration and continuing for 5 h: in these groups the pressure 1 h after decerebration was taken as 100%. In a group of animals which received a normal diet before the acute experiment, the mean percentage pressure rise at the end of 5 h of aldosterone infusion was 20·0 ± 2·3 (s.e.m.)%. In a group whose drinking water had been replaced with 1% NaCl solution, the mean percentage pressure rise after 5 h was 29·6 ± 3·2. In a group pretreated with a low salt intake, the mean percentage pressure rise after 5 h was 10·3 ± 2·8%. These results show that intravenous infusions of aldosterone at the rate of 6 μg/kg/h can raise arterial pressure in acute experiments, and that varying the sodium intake can alter the responsiveness of the cardiovascular system to the hypertensive action of aldosterone.
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Departments of Surgery and *Physiology, The Medical School, The University, Newcastle upon Tyne, NE1 7RU
(Received 12 September 1974)
CB 154 lowers plasma prolactin levels in animals (Flückiger, 1972) and in man (Lutterbeck, Pryor, Vangor & Wenner, 1971), in which it has been successfully used to treat galactorrhoea (Besser, Parke, Edwards, Forsyth, & McNeilly, 1972) and to suppress puerperal lactation (Varga, Lutterbeck, Pryor, Wenner, & Erb, 1972). Hyperprolactinaemia occurs in a number of clinical disorders (Horrobin, 1974) and CB 154 may also be used in these conditions. However, the metabolic effects of this potentially useful drug have not been fully investigated in man or in animals.
Twenty male Wistar rats weighing 140–160 g were used. Ten were given 1 mg CB 154 (Sandoz batch No. 193 H3) intraperitoneally at 12.00 h the day preceding the experiment, and a second injection of 1 mg was given at 08.30 h on the
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In Cushing's syndrome, deoxycorticosterone acetate causes a saluresis instead of the expected sodium retention (Soffer, Lesnick, Sorkin, Sobotka & Jacobs, 1944). In sheep on a high salt intake aldosterone also can cause a saluresis instead of sodium retention (Burstyn, Horrobin & Manku, 1972). The more usual sodium-retaining action can be restored by treatment with prolactin. In sheep we have therefore tested whether cortisol treatment can cause aldosterone to have a sodium-losing action and whether this can be converted back to a sodium-retaining action by prolactin.
Six dioestrous Merino ewes were studied. They were prepared and treated throughout the experiment with a supplement of 80 mequiv. sodium chloride/day as previously described (Burstyn et al. 1972). Each day urine was collected from each animal for two successive 2-h periods from 12.00 to 14.00 and from 14.00 to 16.00 h. The urine volume and sodium and potassium concentrations (measured by means of a
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SUMMARY
To test the effect of prostaglandin A2 (PGA2) on renal function, infusions of PGA2 (0·7 ng/ kg/min), arginine-vasopressin (AVP) (1·25 ng/kg/min) and PGA2 plus AVP were administered to male rats made resistant to the antidiuretic effect of AVP by pre-treatment with lithium. In non-lithium-treated control rats, AVP had its expected antidiuretic action but in lithium-treated rats neither urinary volume nor osmolarity was changed. Prostaglandin A2 alone had no effect on urine output in lithium-treated rats; AVP plus PGA2 infused together evoked a near normal antidiuretic response. This antidiuretic action of PGA2 contrasts with the diuretic action reported by others. However, our infusion rates were 300–4000 times lower than those of other workers and it is suggested that PGs may have opposite actions on the kidney depending on their concentration.
The effect of indomethacin (a blocker of prostaglandin synthesis) on urine flow was tested in five groups of rats on different régimes of liquid intake. Urine flow was reduced in the three groups with the highest urine volumes before treatment, and increased in the two groups with the lowest urinary volumes, again indicating that PGs may have both diuretic and antidiuretic actions.
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In a recent study of renal function in supposedly pregnant rabbits, much time and effort was wasted because about half the mated females failed to become pregnant. On retrospective analysis, the daily sodium excretion was different in the animals which became pregnant as compared with those which failed to become pregnant and which were presumably pseudopregnant. The main difference was apparent on day 4 after mating. We are now using sodium excretion as a simple diagnostic test of pregnancy in rabbits.
Fifteen animals were kept in metabolism cages for 20 days before mating and for the duration of the supposed pregnancy. Only eight of the 15 actually became pregnant. All the urine excreted by each animal each day was collected, its volume measured and its sodium concentration estimated by flame photometry. For each animal the mean daily excretion during the 20-day control period was defined as 100%. Figure 1 shows
