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SUMMARY
Vasopressin content and the staining of neurosecretory material with chrome-alum-haematoxylin-phloxin were observed in the neurohypophysis of rats following injection of formalin. The amount of neurosecretory material was reduced during the period up to 90 min. after formalin injection while no change in the vasopressin content was observed. These observations support the concept that the neurosecretory material is distinct from vasopressin and may be acting as a carrier or precursor for the hormones of the neurohypophysis.
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Abstract
In this study arginine vasopressin (AVP) and oxytocin (OT) receptors have been characterized in the brushtail possum. AVP receptors were characterized using [3H]AVP and the radioiodinated AVP V1a receptor antagonist 125I-labelled [(C6H5-CH2CO)-O-methyl-d-Tyr-Phe-Gln-Asn-Arg-Pro-Arg-Tyr- NH2] while OT receptors were characterized using the radioiodinated OT receptor antagonist 125I-labelled d(CH2)5[Tyr(Me)2,Thr4,Orn8, Tyr-NH2 9]-vasotocin. The receptor affinities and densities have been compared with the rat AVP and OT receptors. Low densities of OT receptors were present in the possum ovary and kidney. High densities of AVP-binding sites were found in the possum adrenal, testis, mesenteric artery, ovary and renal medulla and lower densities in the possum liver. The AVP-binding sites showed marked differences in ligand-binding characteristics from the rat AVP V1a and V2 receptors. Receptor affinities were similar between tissues, except for a distinctly lower value in the renal medulla. It is concluded that the brushtail possum expresses AVP receptors with distinct ligand specificities from those of the rat AVP V1a and V2 receptors.
Journal of Endocrinology (1995) 144, 19–29
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ABSTRACT
A series of studies has been performed in the conscious rat to investigate the effect of the intracerebroventricular (i.c.v.) administration of the selective κ-opioid receptor agonist, U50 488H, on arginine vasopressin (AVP) secretion stimulated by i.c.v. administration of hypertonic NaCl. Similarly, the effect of the i.c.v. administration of morphine and the i.v. administration of naloxone on AVP secretion was investigated. The response of AVP to an i.c.v. injection of hypertonic NaCl was potentiated by naloxone at a dose of 0·4 mg/kg, but a higher dose (1·2 mg/kg) was required to increase the basal plasma concentration of AVP. Prior treatment with U50 488H or morphine attenuated the increase in plasma concentrations of AVP stimulated by i.c.v. injection of hypertonic NaCl from 13·92±4·44 to 1·22±0·34 and 1·78±0·74 pmol/l respectively (n = 7; P<0·05). Prior administration of U50 488H also attenuated the potentiating effect of naloxone on AVP secretion stimulated by i.c.v. injection of hypertonic NaCl. These results indicate that basal AVP secretion is under tonic inhibitory control by dynorphin, and that μ-and κ-opioid receptors mediate an inhibitory influence of endogenous opioids on osmoreceptor-mediated AVP secretion.
Journal of Endocrinology (1991) 129, 411–416
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ABSTRACT
The rat kidney and brain are major target organs for vasopressin (VP). A procedure was developed for immunocytochemical staining of VP and its binding sites in the kidney. This procedure involved preincubation of kidney sections with the ligand, followed by immunocytochemical detection of VP.
The staining in renal tubules from Wistar rats was enhanced by preincubation of tissue sections with increasing concentrations of VP (6–6000 nmol/l). Staining was present in the epithelium of distal convolutions and collecting ducts (medullary and cortical portions) and more pronounced in the apical zone of the tubular epithelium. With high concentrations of VP in the preincubation, staining was also obtained in the thick ascending limb of the loop of Henle. There was no staining under any circumstances in proximal tubules. In the kidney of the Brattleboro rat homozygous for hypothalamic diabetes insipidus (DI) which congenitally lacks VP but responds to the peptide, exactly the same staining pattern was observed after preincubation with VP, but the maximal staining was less intense. The VP binding to the DI rat kidney, after 2 weeks treatment with VP (using Accurel implants), reached levels seen in the Wistar kidney after in-vitro preincubation with high doses of VP.
J. Endocr. (1985) 105, 133–140
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ABSTRACT
Observations were made of fluid balance and vasopressin concentrations throughout the oestrous cycle of normally cyclic female rats housed under a 12 h light: 12 h darkness regime. Plasma vasopressin concentrations were found to increase progressively during the light period, falling again during the night on all days of the cycle except pro-oestrus. On this day, peak vasopressin concentrations of 3·32 ± 0·8 pmol/l were seen between 10.00 and 12.00 h, with lower concentrations of 1·74± 0·22 pmol/l being seen between 18.00 and 19.00 h. Urine flow appeared to reflect the changes in plasma vasopressin concentrations, being significantly lower during the light phase, with a small increase being seen over this period on pro-oestrus. Pituitary vasopressin concentrations were highest between 09.00 and 10.00 h and fell progressively over each of the 4 days of the oestrous cycle. The changes in pituitary content were greater than could be accounted for in terms of the alterations in the plasma concentrations of vasopressin.
J. Endocr. (1988) 117, 397–402
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Plasma vasopressin, arterial blood gas tensions, pH, arterial blood pressure, heart rate and respiration were monitored in conscious rats breathing room air or exposed to varying degrees of hypoxia. A similar series of observations was made in a group of anaesthetized rats and in rats treated with α- and β-adrenergic and dopaminergic blocking agents. The effect of two opioid antagonists on the vasopressin response was also noted. Hypoxia produced an increase in circulating vasopressin concentrations in both conscious and anaesthetized rats. In the conscious animals the increase reached statistical significance when the animals were exposed to 12% oxygen in nitrogen, which produced a fall in arterial PaO2 of 44·7 ± 5·0%. Guanethidine, phentolamine and propranolol all produced a significant fall in the basal concentrations of vasopressin, while guanethidine, phenoxybenzamine and propranolol blocked the increase seen on breathing 12% oxygen in nitrogen. Naloxone and levallorphan also reduced the vasopressin response to hypoxia. Thus it appears that aminergic pathways play a role in the maintenance of circulating concentrations of vasopressin and in the response to hypoxia. Endogenous opioids also appear to be involved in the hypoxic response.
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ABSTRACT
The inhibition of γ-aminobutyric acid (GABA) synthesis did not interfere with the suppressive effect of dexamethasone on the stress-induced rise of plasma corticosterone levels in vasopressin-deficient homozygous Brattleboro rats. In dexamethasone-treated heterozygous rats corticosterone and vasopressin secretion increased after stress provided GABA synthesis was inhibited. The results indicate that inhibition of corticotrophin secretion by corticosteroids may in part be mediated by enhancement of GABA synthesis and a consequent inhibition of vasopressin release.
J. Endocr. (1985) 107, 303–307
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SUMMARY
A radioimmunoassay has been developed for plasma arginine-vasopressin in man and dog. The mean recovery of added arginine-vasopressin (AVP) was 60 ± 6·9 (s.d.)% and the lower threshold of detection 2·0 pmol/l. A close correlation was found between concurrent radioimmunoassay and bioassay values. The mean concentration found in peripheral venous blood in healthy men after overnight fasting was 5·3 pmol/l (range 4·6–6·2 pmol/l). In man, significant increases in plasma AVP occurred after dehydration (5·9–9·5 pmol/l) and significant decreases after oral water-loading (5·2–3·7 pmol/l). During i.v. infusion of graded doses of synthetic AVP in normal men, plasma levels were closely correlated with infusion rate. On stopping the infusion, plasma vasopressin fell exponentially with a half-life of between 7 and 8 min. In man, plasma AVP was unaffected by tilting head-up for 2 h, or by a non-hypotensive bleeding of 500 ml in 10 min. In the dog, haemorrhage of 5 ml/kg and over caused proportionate increases in AVP in the circulation. In normal men, plasma vasopressin was significantly correlated with concurrent urinary osmolality. Five patients with oat-cell bronchial carcinoma and hyponatraemia showed a marked increase of plasma vasopressin. Five patients with diabetes insipidus had significantly reduced, but detectable, levels of plasma AVP. The plasma concentration in these patients did not increase after water restriction.
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SUMMARY
The isolated dog kidney was perfused with blood containing 1 m-u. arginine vasopressin/ml. In other experiments 40 or 50 m-u./min. were infused into three intact dogs. Antidiuretic activity was measured in renal venous blood, arterial blood, and in the urine. Renal blood flow was determined directly in the perfused dog kidney and by p-aminohippuric acid clearance in the intact dog; glomerular filtration rate was measured by either inulin or creatinine clearance.
About 38% of the hormone was extracted from the arterial blood in its passage through the kidney. Of the total amount of hormone infused, about 18% was eliminated by each kidney. The quantity of vasopressin extracted from the blood was greater than that excreted in the urine, indicating that the hormone is inactivated by the kidney. In intact dogs, the amount of hormone filtered by the kidney was less than that excreted, suggesting tubular secretion.
It was calculated that the release of endogenous arginine vasopressin induced by the stimuli of anaesthesia and surgery was between 3 and 7 m-u./min. and that approximately 15% of the endogenous hormone was excreted.
Ultrafiltration of dog plasma at three different concentrations of arginine vasopressin (30, 100 and 290 μ-u./ml.) showed that binding was reduced as the concentration was raised and that at the concentration of hormone in the experiments, less than 30% was bound.
The difficulties of relating these findings at artificially high blood concentrations to those at physiological blood concentrations of vasopressin are discussed.
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Estimations of urine volumes and inulin U/P ratios in newborn rats after the administration of 4·5 ml. water and 10 mU. vasopressin/100 g. body weight failed to show an antidiuretic response comparable to that produced in adult controls. When body surface was chosen as the basis of dosage, relatively larger amounts of water were given to newborn rats. These produced an increase in the rate of urine flow (which, however, still remained well below the adult level), but an inhibitory effect of vasopressin again could not be demonstrated.
Experiments on older rats (up to 4 weeks of age) showed that an antidiuretic effect of vasopressin comparable to that of adults develops only after several weeks of postnatal life, approximately at the same time as a full diuretic response to water could be obtained.
When 10 mU. vasopressin/100 g. body weight was injected both adult and newborn rats excreted about 10% of this dose.
It is suggested that vasopressin acts less effectively in newborn rats because for some time after birth the kidney is less responsive to the posterior pituitary antidiuretic hormone than in adults.
