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It appears likely that the blood concentration of arginine vasopressin in man in normal water balance is less than 1·5 μ-u./ml. (Bisset & Lee, 1958; Moran, Miltenberger, Shuayb & Zimmermann, 1964). Any attempt to assay this small quantity requires a very sensitive preparation, or a method of extraction which will concentrate the hormone with little loss, or both. Heller & Štulc (1959) have reported that if the urinary bladder was exteriorized several days before using rats for assay and if a needle was inserted into the tail vein on the day of the experiment, the rat would respond to 0·625 μ-u. of vasopressin, an increase of sensitivity about fivefold greater than previously reported. Czaczkes, Kleeman & Koenig (1964) confirmed these results using female Sprague-Dawley rats weighing 100–120 g.; a water-ethanol load was maintained by infusion into the tail vein. Urine flow was measured every 10 min.
We have followed this procedure
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SUMMARY
The preparation is described of a hormone-binding protein fraction from bovine neurohypophyses (neurophysin). The fraction obtained by ion-exchange chromatography on CM-cellulose contained two components which were separated by gel filtration on Sephadex G-75; the property of binding oxytocin and arginine vasopressin was possessed by only one component of which the molecular weight was 25,000 approximately. The capacities of this protein to bind oxytocin and arginine vasopressin (each hormone in the absence of the other) were studied by a film dialysis method. The maximum binding capacities were 125 units of oxytocin/mg. protein and 62 units of arginine vasopressin/mg. protein, which are equivalent to seven molecules of oxytocin and four molecules of arginine vasopressin/molecule of protein (taken to the nearest whole numbers).
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SUMMARY
The oxygen consumption of toad urinary bladders was lower in preparations made up as sacs than in pieces of tissue freely suspended in Ringer solution.
Vasopressin stimulated uptake of oxygen by both types of preparation. This probably reflects facilitated sodium transport from the mucosal to serosal side of the tissue since exclusion of this ion from the fluid bathing the mucosa (inside) abolished this effect.
When water transfer across the bladder is promoted by vasopressin (in the presence of an osmotic gradient; inside hypo-osmotic) there is a reduction (by about 50%) in usage of oxygen. Cyclic AMP had a similar action.
Theophylline and cyclic AMP failed to influence oxygen uptake by pieces of toad bladder tissue freely bathed in sodium—Ringer solution. In preparations made as sacs containing iso-osmotic sodium—Ringer solution the nucleotide stimulated while, paradoxically, the xanthine depressed oxygen consumption. This action of cyclic AMP (like that of vasopressin) is dependent on the presence of sodium at the mucosal side of the tissue since it is not seen in sacs filled with choline—Ringer solution. However, the reduction in O2 consumption produced by theophylline was still seen in the absence of sodium.
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Abstract
The renal actions of vasopressin were studied in the conscious female rat. Vasopressin caused a dose-dependent increase in sodium excretion when administered at 40–160 pmol/min. The highest dose, which increased sodium excretion from 10·4 ± 0·3 μmol/min (n=32) to 18·3 ± 0·8 μmol/min (n=8, P<0·001), also caused a significant rise in glomerular filtration rate (GFR). The antidiuretic and natriuretic responses to vasopressin varied significantly over the 4 days of the oestrous cycle. Both responses were greatest on pro-oestrus, being −57 ± 3 and 52 ± 3% above the control values with 80 pmol vasopressin/min. Responses of similar magnitude were also seen on dioestrus day 1. On these two cycle days the effects on urine flow and sodium excretion were accompanied by a significant increase in GFR. Smaller antidiuretic and natriuretic responses were seen on oestrus and dioestrus day 2, without concomitant changes in GFR. As the plasma vasopressin concentrations produced by hormone infusion were similar on each day of the cycle, the renal responsiveness to vasopressin appears to vary over the 4 days of the oestrous cycle. This may be important in terms of alteration and possible disturbances of fluid balance which may occur during reproductive cycles and pregnancy.
Journal of Endocrinology (1996) 148, 457–464
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Abstract
Experiments were done to study the effects of porcine relaxin on osmotically evoked changes in intramammary pressure and the release of oxytocin and vasopressin in anaesthetized rats. Injections (1 μ1) of hypertonic (0·75 m) NaCl into the left lateral cerebral ventricle were used to induce consistent rises in intramammary pressure and the release of oxytocin and vasopressin. Plasma hormone concentration was determined by radioimmunoassay. Relaxin (5 μg i.v.) significantly (P<0·05) suppressed the intramammary pressure response to osmotic challenge 5 and 10 min after treatment. However, pretreatment with a specific vasopressin V1 receptor antagonist completely negated the effect of relaxin on intramammary pressure. Baseline levels of oxytocin and vasopressin in unstimulated rats were 41 ± 1·6 and 36±1·1 pmol/l respectively. Osmotic challenge induced significant (P<0·05) rises in plasma levels of both hormones (62·8 ±1·1 and 67·9 ± 1·2 pmol/l respectively) which were further augmented by relaxin (81·3±1·8 and 117·1 ±2·4 pmol/l respectively; P<0·05). The data confirm that central osmotic challenge provokes the release of oxytocin and vasopressin but the effects of oxytocin at the level of the mammary gland may be obscured by the action of vasopressin affecting blood flow to the gland.
Journalof Endocrinology (1994) 141, 75–80
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ABSTRACT
The vasopressin response of rats to i.p. injection of hypertonic sodium chloride (1·5 mol/l) was compared with that following i.v. infusion of 1·05 mol sodium chloride/l. The two regimes produced a similar vasopressin response in terms of the osmotic threshold, although the slopes of the plot of plasma vasopressin levels against plasma osmolality were not identical. Pretreatment with naloxone and levallorphan increased the resting vasopressin levels and effectively potentiated vasopressin release in response to hypertonic saline by reducing the osmotic threshold for hormone release. Thus, opioid peptides appear to exert an inhibitory effect on vasopressin release under resting and stimulated conditions. The adrenoreceptor antagonists propanolol, phenyoxybenzamine and phentolamine produced a fall in resting vasopressin concentrations while propanolol and phenoxybenzamine potentiated the osmotic release of vasopressin in association with a fall in the osmotic threshold. This would suggest that noradrenergic pathways are excitatory at rest while having an inhibitory effect on the osmotic response. Metoclopramide also produced a fall in resting plasma vasopressin concentrations while increasing the osmotic response. In contrast haloperidol did not affect the vasopressin response.
J. Endocr. (1988) 116, 217–224
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ABSTRACT
Glucocorticoids are known to inhibit the ACTH response to a variety of stimuli. It has been suggested that vasopressin secretion is also inhibited by glucocorticoid negative feedback. The purpose of this study was to (1) determine the ACTH response to hypertonic saline and its sensitivity to glucocorticoid negative feedback and (2) to determine whether physiological elevations of plasma cortisol inhibit subsequent vasopressin responses to hypertonic saline. Five mongrel dogs (15–18 kg) were prepared with chronic arterial and venous catheters and studied while conscious. Ten experiments were performed on each dog in a randomized design separated by at least 5 days. Each experiment consisted of a pretreatment period (from −60 to −30 min except for dexamethasone administration) during which a glucocorticoid feedback signal was applied and a stimulus period (from 0 to 30 min) during which hypertonic saline was infused. The pretreatment and stimulus periods were separated by 30 min. Pretreatments were as follows: isotonic saline (control), half-maximal and maximal cortisol infusion (5·5 or 11 nmol/kg per min), ACTH(1–24) infusion (6·8 pmol/kg per min) which produces increases in endogenous cortisol, and dexamethasone (1·5 mg i.m.) given at 17.00 h the day before experimentation. Stimuli were as follows: hypertonic saline was infused at 0·2 or 0·4 mmol/kg per min which increased plasma sodium by about 6 or 12 mmol/l respectively. NaCl infusion at 0·2 mmol/kg per min had no effect on plasma ACTH or cortisol except when subsequent to ACTH(1–24) pretreatment when plasma ACTH actually increased to 41·4 ± 2·9 pmol/l in response to hypertonic saline. NaCl infusion at 0·4 mmol/kg per min resulted in a significant increase in plasma ACTH from 5·9 ± 0·9 to 11·7 ± 2·0 pmol/l in the control group. This ACTH response was blocked by pretreatment with either dose of cortisol and dexamethasone. ACTH pretreatment, however, did not completely block the ACTH subsequent response to infusion of 0·4 mmol NaCl/kg per min. The two doses of NaCl led to significant and dose-related increases in plasma vasopressin. None of the pretreatments significantly affected the vasopressin response to hypertonic saline except for significant inhibition after overnight dexamethasone. We conclude that (1) hypertonic saline can stimulate ACTH release if plasma sodium is increased sufficiently, (2) the ACTH response to hypertonic saline is potentiated by pretreatment with ACTH making it different from other stimuli studied previously, and (3) the vasopressin response to hypertonic saline is not inhibited by short-term elevations of plasma cortisol within the physiological range.
Journal of Endocrinology (1989) 122, 41–48
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Division of Pharmacology and Therapeutics, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 1N4, Canada
(Received 13 June 1977)
Several lines of circumstantial evidence suggest that the neurohypophysial hormones may be biosynthesized in the form of larger peptides (prohormones) which are degraded to the free hormones during passage of the neurosecretory granules from the hypothalamus to the neurohypophysis (Vogt, 1953; Sachs & Takabatake, 1964; Pickering, Jones & Burford, 1971). Furthermore, it has been suggested that the hormone carrier proteins, the neurophysins, may at some stage in the biosynthesis, form part of the putative prohormones (Hope & Pickup, 1974).
In cattle, arginine-vasopressin (AVP) is associated with bovine neurophysin II (Dean, Hope & Kazič, 1968), the complete amino acid sequence of which has been elucidated by Schlesinger, Capra & Walter (1974) and Wuu & Crumm (1976). In the present study, two dodecapeptide analogues of AVP in which the peptide chain was elongated
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ABSTRACT
Immunoreactive vasopressin and oxytocin were measured in the hypothalamo-hypophysial portal blood of both Long–Evans and homozygous Brattleboro rats. Adrenalectomy caused an increase in vasopressin immunoreactivity in portal blood in the Long–Evans strain, whilst administration of dexamethasone to these adrenalectomized animals resulted in a reduction in portal vasopressin immunoreactivity to levels below those seen in sham-operated animals. This vasopressin immunoreactivity co-eluted with synthetic vasopressin on high-pressure liquid chromatography (HPLC), and diluted in parallel in radioimmunoassay. In Brattleboro rats, however, although vasopressin-like immunoreactivity was detected, the portal concentration did not vary with the adrenal status of the animal, nor did it show the characteristics of standard vasopressin on HPLC or in immunoassay. Oxytocin was present in the portal blood of both Long–Evans and Brattleboro rats at similar very high concentrations, but did not vary in response to adrenalectomy. These results are consistent with a role for vasopressin, but not oxytocin, in the hypothalamic response to adrenalectomy and glucocorticoid feedback. Neither vasopressin immunoreactivity nor oxytocin appear to subserve this role in the homozygous Brattleboro rat.
J. Endocr. (1988) 117, 27–34
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Abstract
The effect of three oxytocin receptor antagonists on the renal actions of oxytocin and vasopressin was investigated in conscious male rats infused with hypotonic saline. Infusion of oxytocin at 100 pg/min produced plasma concentrations of 12·7 ± 3·3 pmol/l and led to significant increases in sodium excretion, urine flow and glomerular filtration rate (GFR). The increase in sodium excretion of 42 ± 9% during oxytocin infusion was significantly decreased by all three antagonists to 15 ± 5% (10 ng [mercapto-proprionic acid1,d-Tyr(Et)2, Thr4,Orn8]-oxytocin/min), 13 ± 5% (5 ng desGly9[d-Trp2,Thr4,Orn8]-dC6oxytocin/min) and 4 ± 5% (1 ng d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr(NH2)9]-vasotocin/min). Similarly, the increase in urine production of 22 ± 5% associated with oxytocin infusion was significantly decreased to 4 ± 3% (5 ng desGly9[d-Trp2,d-Thr4,Orn8]-dC6oxytocin/min) and 1 ± 4% (1 ng d(CH2)5[Tyr(Me)2,Thr4,Orn8,Tyr(NH2)9]-vasotocin/min). All three antagonists blocked the oxytocin-induced increase in GFR when infused at 10 ng/min. Infusion of vasopressin at 160 pg/min produced plasma concentrations of 10·1 ± 2·1 pmol/l and this led to a significant increase in sodium excretion and a significant decrease in urine flow rate. None of the antagonists had any effect on the natriuretic or antidiuretic actions of vasopressin suggesting that different receptors are involved in these renal actions of the two peptides.
Journal of Endocrinology (1997) 152, 257–264
