1. A new rat model has been developed allowing body fluid status to be accurately controlled and maintained throughout experimentation by computer-driven, servo-controlled replacement of spontaneous urinary fluid losses. 2. Experiments in vitro were performed to test the accuracy of the servo system, and experiments in vivo were carried out to re-assess basic renal function in servo-controlled vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats. The model was further evaluated in water-diuretic Wistar rats with or without administration of a vasopressin V 2 -receptor agonist, 1-desamino-8- d -arginine vasopressin. 3. The data gained from the present study indicate the suitability of the servo-controlled replacement system for conscious renal function studies in three different rat strains. Haemodynamic and renal function variables measured were demonstrated to be stable throughout a 5 h experimental procedure and reproducible between repeated experimental occasions over a 14 day post-operative period. 4. Using the servo-control technique, the expected action of 1-desamino-8- d -arginine vasopressin on renal water handling was demonstrated, but the natriuretic effect reported by some workers was not evident. 5. Since the servo-controlled fluid replacement technique maintains many of the inherent differences between vasopressin-replete Long Evans and vasopressin-deficient Brattleboro rats and eliminates the changes in body fluid volume during transition from a diuretic to an antidiuretic state, the model confers an advantage over previously employed constant infusion protocols.
1. The influence of gonadal and pituitary factors on the plasma renin response to exogenous vasopressin was examined in anaesthetized rats. 2. Plasma renin activity (PRA) was measured in Brattleboro rats (with and without hypothalamic diabetes insipidus) and Long-Evans male and female rats, before and after single intravenous injection of antidiuretic hormone (ADH) or saline. 3. Control saline injections did not change PRA. ADH reduced PRA in male, but increased PRA in female rats. Rats with diabetes insipidus displayed the greatest changes and were used in subsequent experiments. Extrarenal renin activity (nephrectomized rats) gave qualitatively similar responses to ADH. Plasma renin concentration, which was also measured with PRA in intact and nephrectomized male and female rats with diabetes insipidus, increased in the females and decreased in the males after ADH. 4. Castration, 24 h before study, abolished the ADH-induced fall in PRA, and testosterone implanted before castration did not restore the response. Cyproterone acetate reversed the ADH effect in males, so that PRA then rose after ADH. Hypophysectomized male rats, with depressed basal plasma renin activities, also showed a reduced PRA after ADH. 5. Ovariectomy had little effect on the ADH-induced renin release and the response was similar at oestrus, metoestrus and dioestrus. In hypophysectomized female rats ADH reduced PRA; a male pattern of response was seen in hypophysectomized female rats. 6. In both sexes PRA responses to ADH were blunted but not abolished by β-adrenergic blockade (propranolol). α-Adrenergic blockade (phenoxybenzamine) had little influence on the male response but in females the typical increase disappeared so that ADH reduced PRA. 7. It is concluded that pituitary hormones, including gonadotrophins and gonadal factors as well as adrenal sex steroids, appear to affect significantly the interplay between antidiuretic hormone and the renin—angiotensin system.