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Plasma vasopressin concentrations, determined by radioimmunoassay, were followed throughout the menstrual cycle in eight healthy women. The concentrations were found to depend on the day of the menstrual cycle. The mean concentration on day 1 was 0·5±0·08 (s.e.m.) μu./ml, while that on days 16–18 was 1·1±0·16 μu./ml. These values were significantly (P <0·02) different. Vasopressin release in women may thus depend on the hormonal changes during the menstrual cycle.
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SUMMARY
The infusion of vasopressin in amounts thought to be released during water deprivation had no effect on the rate of milk secretion or on milk composition. These results do not support the conclusions of Konar & Thomas (1970) that vasopressin at physiological levels affects the rate of milk secretion, since the doses they used were very much higher and probably outside the physiological range. The implications of these findings and their possible adaptive significance are discussed.
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ABSTRACT
The mechanism of water conservation is impaired in ageing mammals. An age-related defect in the release of vasopressin has been implicated but, more recently, attention has moved to the renal component of the water conservation mechanism. Previous studies using renal cells prepared from mice of different ages have shown that the threshold dose of vasopressin required to elicit a significant rise in cyclic AMP (cAMP) was greater in older animals. The dose–response curve was moved to the right in 35-month-old mice, i.e. the concentration of vasopressin required to give maximum cAMP output was increased. To investigate this further we examined the binding of vasopressin to renal medullary cells maintained in short-term culture, to determine whether the decreased response of cAMP levels to vasopressin is due to changes in hormone-receptor interaction. In 6-month-old male mice the dissociation constant (K d) was 2·38 nmol/l and the maximum binding of the hormone (Bmax) was 47·6 fmol/106 cells, and at 30 months of age K d was 2·37 nmol/l and Bmax was 47·0 fmol/106 cells. In female mice the changes were more complicated because the data for the 6-month-old mice could be split into two groups. It is concluded that there are no age-related differences in the numbers of receptors or their affinity for vasopressin, and that the decreased cAMP response is probably associated with post-receptor mechanisms in this species.
J. Endocr. (1987) 115, 379–385
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The concentrations in plasma of triglycyl-8-lysine-vasopressin (TGLVP), determined by radioimmunoassay, and lysine-vasopressin, determined by bioassay, have been monitored in five subjects after intravenous (7·5 μg/kg) or intranasal (5 mg) administration of TGLVP. The level of excretion in urine was also measured. The TGLVP concentration in plasma fell rapidly after the intravenous injection, the mean half-time of disappearance being 24·2±1·9 (s.e.m.) min (d.f. 4). Biologically active lysine-vasopressin reached a peak between 60 and 120 min. A similar pattern was seen following intranasal instillation but only a small proportion of the administered dose appeared in the plasma and the concentration of lysine-vasopressin was relatively higher. Less than 1% of the TGLVP injected appeared in the urine. Intravenous TGLVP had no effect on systolic blood pressure but produced an increase in diastolic blood pressure of 1·7 ± 0·19 kPa (d.f. 4) and a fall in heart rate of 9 ± 2·3 beats/min. Creatinine clearance and sodium excretion remained relatively constant in all subjects throughout the study but intravenous injection of TGLVP resulted in an antidiuresis which was evident within the first hour of observation and was maintained for a further 4 h. It was concluded that TGLVP is converted to lysine-vasopressin in man and after an intravenous injection of 7·5 μg/kg sufficiently high concentrations of lysine-vasopressin may be maintained for 2 h to produce sustained vasoconstriction. Triglycylvasopressin may therefore be of value in controlling haemorrhage.
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Studies were carried out to determine whether endogenously secreted vasopressin in the circulation of the dog is freely filterable. Blood from anaesthetized dogs was pumped through a dialysis coil and ultrafiltration was achieved by increasing the outflow pressure from the coil. In some cases, the dogs were hydrated before the experiment. A specific, precise radioimmunoassay was used to measure the concentration of vasopressin in the ultrafiltrate and the simultaneously sampled plasma. The concentration of vasopressin in the ultrafiltrate was consistently lower than that in the plasma at concentrations ranging from 1·7 to 335 μu./ml in the latter, and the extent of the binding was lower in the hydrated than in the non-hydrated dogs. At plasma levels of vasopressin of 2–20 μu./ml, vasopressin binding averaged only about 12%, whereas it averaged 40% at plasma concentrations greater than 20 μu./ml. This binding was not an artifact caused by some limitation of the ultrafiltration system because vasopressin dissolved in a salt solution and subjected to ultrafiltration in the system was freely filterable.
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Introduction Vasopressin (AVP) and corticotropin-releasing hormone (CRH) are the two main neuropeptides regulating the hypothalamic–pituitary–adrenal (HPA) axis. AVP, secreted from parvocellular neurons of the paraventricular nucleus (PVN) of the
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The passage of 125I-labelled arginine-vasopressin (AVP) and its analogues desmopressin (DDAVP) and desglycinamide arginine-vasopressin (DGAVP) into cerebrospinal fluid (CSF) has been studied in the dog. After intravenous injection or infusion of these peptides radioactive sustances were found in the CSF in amounts ranging from 0·5 to 1·4% of the total plasma radioactivity. However, only DDAVP could be identified in the CSF as the unmetabolized peptide. This observation may be related to the long plasma half-life of DDAVP which was found to be 50 min, compared with a half-life of 13 min for AVP and 8 min for DGAVP.
After the intranasal administration of either [3H]AVP or 125I-labelled AVP similar results were obtained. Radioactivity was again present in the CSF but no AVP could be identified. These observations showed that the intranasal route of administration provides no increased access to the CSF.
The existence of a blood–CSF barrier to AVP is confirmed and indicates that the concentrations of the hormone normally found in CSF arise from sources other than the blood.
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Introduction Corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) are the two major regulatory peptides in the hypothalamic–pituitary–adrenal (HPA) axis. CRF, produced in the hypothalamic paraventricular nucleus (PVN
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Introduction
Everyone accepts that the principal physiological action of the neurohypophysial hormone vasopressin is to stimulate the osmotic reabsorption of water by binding to V2 receptors on collecting duct cells. Activation of these G-protein coupled receptors induces the intracellular generation of cyclic AMP and, ultimately, the movement of water across the renal epithelium through water channels inserted into the apical membranes (see Brown 1989). These water channels, called aquaporins, have now been cloned for collecting duct apical membranes in various mammalian species (Fushima et al. 1993).
However, the first observed effect of this antidiuretic hormone was not concerned with the renal action on water transport. In 1895, Oliver and Schäfer showed that extracts of the hypophysis had powerful pressor activity, hence the name given to the active ingredient – vasopressin. Ironically, many people today do not believe that vasopressin has a physiological role in cardiovascular regulation even though it was
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ABSTRACT
The distribution of [3H]vasopressin- and [3H]oxytocin-binding sites was examined, using an autoradiographical technique, in the kidney of Long–Evans and Brattleboro rats. Two types of binding sites with affinities in the nanomolar range were detected: one, located on glomeruli, bound both vasopressin and oxytocin; the other, on collecting ducts, bound vasopressin selectively. In the presence of 10 μmol oxytocin/1, [3H]vasopressin labelling was abolished in glomeruli, but only reduced in collecting ducts; [3H]oxytocin labelling was completely abolished by 10 μmol vasopressin/1. These observations are discussed in relation to known effects of neurohypophysial hormones on renal physiology.
J. Endocr. (1987) 113, 179–182
