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Studies were designed to determine whether angiotensin II has a direct stimulatory effect on arginine-vasopressin in man and to determine the role, if any, played by angiotensin II in the control of vasopressin release in physiological and pathological conditions.
Acute infusion of angiotensin II in normal volunteers produced small but definite increases in plasma levels of arginine-vasopressin (5·4 ± 0·3 (s.e.m.) to 6·4 ± 0·2 pg/ml) only when plasma angiotensin II levels were supraphysiological.
Concurrent measurements of plasma arginine-vasopressin and angiotensin II were made during acute changes in fluid balance and posture in normal volunteers and in clinical conditions characterized by high plasma levels of angiotensin II (Addison's disease and Bartter's syndrome). The results of these studies allow us to conclude that there is little to suggest a direct effect of angiotensin II which is likely to be relevant to the normal physiological control of arginine-vasopressin in man.
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The content of vasopressin, oxytocin and their related neurophysins was measured in the hypothalamus and pituitary gland of mid-trimester human fetuses. Vasopressin was present in both tissues approximately 3–4 weeks before oxytocin. The levels of the hormones in the pituitary gland increased 1000-fold over the next 3–4 months. During this time, the very high vasopressin/oxytocin ratio gradually decreased but did not reach unity in the period studied. In contrast, both the vasopressin-associated neurophysin and the oxytocin-associated neurophysin appeared in the pituitary gland at the same gestational age and showed the same exponential increase with fetal age. Lower levels of the neurophysins and the nonapeptides were found in the hypothalamus and the levels increased more slowly with fetal age. Our results suggest that the high vasopressin/oxytocin ratios observed in fetal life are due to differences in the rate of maturation of the hormone precursor, rather than to differences in the rate of de-novo synthesis.
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Introduction The release of adrenocorticotropic hormone (ACTH) is stimulated by two hypothalamic neuropeptides: corticotropin-releasing hormone (CRH) and arginine-vasopressin (AVP). ACTH release in response to CRH stimulation is
Search for other papers by MARY L. FORSLING in
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Departments of Physiology, *The Middlesex Hospital Medical School, Cleveland Street, London, W1P 6DB, and St Mary's Hospital Medical School, Praed Street, London, W2 1PG
(Received 13 October 1976)
Recently there has been increasing interest in the possible role of foetal neurohypophysial hormones in parturition (Alexander, Bashore, Britton & Forsling, 1974; Burton, Illingworth, Challis & McNeilly, 1974). The significance of plasma levels in the mother and foetus depends on the placental permeability to the hormone. It has been suggested that in the sheep there is no placental transfer of oxytocin (Forsling, Jack & Nathanielsz, 1975) or arginine-vasopressin (AVP) (Alexander et al. 1974). Burton and her co-workers, however, reported that the guinea-pig placenta allows passage of oxytocin. It is therefore of interest to know whether this placenta which is haemochorial in nature is also permeable to AVP.
The placentae of nine guinea-pigs in the third trimester of pregnancy were perfused by recirculation
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ABSTRACT
The purpose of this study was to determine the effect of water restriction on the vasopressin response to hypoxia in conscious Long–Evans rats. Rats were prepared with chronic indwelling femoral artery and vein catheters 1 week before experimentation. At 24 h before the first blood sample, the supply of drinking water was maintained ad libitum (water replete) or removed (water deplete). At 24 h, a control blood sample was taken and then normoxia (21% O2) was maintained or hypoxia (10% O2) induced. Additional blood samples were taken at 1, 18 and 24 h. All blood samples (2·5 ml) were simultaneously replaced with donor blood to maintain isovolaemia. Hypoxia led to a very small and transient increase in vasopressin in the water-replete rats. The combination of hypoxia and water restriction led to a greatly augmented vasopressin response at 1 h (60 ± 16 pmol/l); this response was also not sustained. Additional non-cannulated rats were exposed to 24 h of normoxia or hypoxia with or without water available ad libitum and posterior pituitaries were collected after decapitation for measurement of vasopressin content. Water restriction, hypoxia and water restriction plus hypoxia all led to decreased pituitary vasopressin content. We conclude that the vasopressin response to hypoxia in conscious rats is small and transient, and that concomitant water restriction augments the vasopressin response to acute but not chronic hypoxia.
Journal of Endocrinology (1990) 125, 61–66
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A long-lasting and constant release of vasopressin in serum solution (in vitro) for periods up to 50 days can be obtained by the use of small-diameter microporous Accurel polypropylene tubing, filled with vasopressin and covered with collodion. The potency of the preparation is shown in vivo after subcutaneous implantation in the adult vasopressin-deficient Brattleboro rat, for which normal levels of urine production and osmolality were achieved at least for 1 month. The possible use of this method for other peptides and its application in small or immature laboratory animals and in fetuses is emphasized.
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Netherlands Central Institute for Brain Research, Ijdijk 28, Amsterdam-0, The Netherlands
(Received 3 July 1975)
The 'classical' view on the distribution of oxytocin and vasopressin producing cells suggests that the paraventricular nucleus (PVN) is predominantly or entirely responsible for oxytocin production and the supraoptic nucleus (SON) synthesizes mainly vasopressin. However, recent hormone assays and electrophysiological studies indicate the presence of each hormone in both nuclei (for references see Burford, Dyball, Moss & Pickering, 1974). We report an immunofluorescence study in the SON and the magnocellular part of the PVN (Bodian & Maren, 1951) using antibodies to oxytocin (produced in our laboratory) and to vasopressin (produced by Drs Hollemans, Schellekens and Touber), purified by absorption with arginine-vasopressin and oxytocin respectively (Swaab & Pool, 1975).
Frontal cryostat serial sections of glyoxal-prefixed hypothalami from five male Wistar rats weighing 200 g were studied. Out of each group of six sections, the first was
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Nuffield Institute for Medical Research, University of Oxford, Oxford, 0X3 9DS
(Received 11 March 1976)
Vasopressin is considered an important hormone controlling adrenocorticotrophin (ACTH) secretion under some conditions (De Wied, Bohus, Ernst, de Jong, Nieuwenhuizen, Pieper & Yasumura, 1968). Its infusion into dogs at pharmacological but not physiological doses increases plasma ACTH concentration (Andersen & Egdahl, 1964). It behaves as a corticotrophin-releasing factor on incubation with anterior pituitary cells (Portanova, Smith & Sayers, 1970). Moreover a neuroendocrine vasopressin pathway possibly associated with ACTH secretion has been proposed (Parry & Livett, 1973). During hypoxaemia in the foetal sheep there is a rise in both plasma ACTH and vasopressin (Alexander, Britton, Forsling, Nixon & Ratcliffe, 1973; Boddy, Jones, Mantell, Ratcliffe & Robinson, 1974b; Rurak, 1976). Thus the possibility that a rise in foetal plasma vasopressin is responsible for the increased secretion of ACTH during hypoxaemia has been investigated. Foetal and maternal vascular
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ABSTRACT
Blood samples were collected twice daily (09.30 and 17.00 h) via indwelling jugular-vein cannulae from five ewes throughout an entire oestrous cycle. Additional frequent samples were taken at 30-min intervals for 8 h on each of days 3 (early luteal phase), 9 (mid-luteal phase), 12 (late luteal phase) and 0 (day of oestrus). Plasma concentrations of arginine vasopressin and oxytocin were measured in all samples by radioimmunoassay and progesterone was measured in the twice-daily samples only.
Both oxytocin and progesterone showed the expected pattern of plasma concentrations, increasing during the early luteal phase, reaching a plateau and declining either preceding (oxytocin) or at (progesterone) luteolysis. Vasopressin concentrations showed a significant dependence on the day of cycle (P<0·05, analysis of variance) with concentrations lowest at oestrus and minor peaks on days 4 and 8–9. There was no correlation between the concentrations of vasopressin and progesterone. Vasopressin values were significantly higher in the morning than in the afternoon samples (1·3 cf. 0·9 pmol/l; P<0·001). Analysis of the frequent samples showed a significant (P<0·001) dependence on the time of day for vasopressin but not oxytocin. Values were high throughout the morning, declined to a trough at 15.00 h and rose again by 17.00 h.
We conclude that there is a minor variation in the vasopressin concentration during the oestrous cycle, which is not related to the circulating progesterone concentration but could be regulated by oestradiol. We also provide evidence for a diurnal rhythm in the release of vasopressin into the plasma in the ewe. The concentrations of vasopressin measured are unlikely to be sufficient to influence the activity of the reproductive tract in vivo.
Journal of Endocrinology (1992) 134, 107–113
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Abstract
The renal effects of arginine vasopressin and oxytocin were studied in the conscious unrestrained rat infused with 0·077 m NaCl. Peptides were infused at rates of 24 and 160 pmol/min (vasopressin) or 30 and 200 pmol/min (oxytocin) either alone or as a combination of the two lower or two higher doses. The rates of infusion were selected to give ratios of oxytocin:vasopressin similar to those seen in the plasma of euhydrated and dehydrated rats.
Vasopressin produced dose-dependent antidiuretic and natriuretic responses, the natriuresis commencing after 15–30 min infusion. Oxytocin produced dose-dependent diuretic and natriuretic responses, the natriuresis commencing within the first 15 min of infusion. Combined infusion of vasopressin and oxytocin produced dose-dependent antidiuretic responses which were comparable to those seen with vasopressin alone. The natriuretic response from combined infusion at the higher rate appeared to have the greater magnitude for individual 15-min periods of the vasopressin response combined with the longer duration of the oxytocin response. Although the total natriuretic response was therefore greater, this difference failed to reach significance.
Only the higher rates of infusion of vasopressin and oxytocin significantly increased the clearance of sodium, by 53 ± 23 and 62 ± 18% and glomerular filtration rate (GFR) by 23 ± 4 and 23 ± 4% respectively. The clearance of sodium during the combined hormone infusion was significantly greater (109 ± 21%), while the rise in GFR at 23 ± 5% was comparable to that seen when each hormone was given separately. Both fractional excretion of sodium and potassium excretion were also significantly elevated by this combined infusion, suggesting an additional tubular component to the response. Although no synergistic effect of neurohypophysial hormones on the antidiuresis was found in the conscious rat, they may act together to promote sodium excretion
Journal of Endocrinology (1995) 144, 441–448
