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Jphysiol00593-0531.Pdf J. Physiol. (1984), 352, pp. 517-526 517 With 2 text-figures Printed in Great Britain NATRIURETIC RESPONSE OF THE RAT TO PLASMA CONCENTRATIONS OF ARGININE VASOPRESSIN WITHIN THE PHYSIOLOGICAL RANGE BY R. J. BALMENT*, M. J. BRIMBLE*, MARY L. FORSLINGt AND C. T. MUSABAYANE* From the *Department of Physiology, University of Zimbabwe, P.O. Box MP 167, Mount Pleasant, Harare, Zimbabwe and the tDepartment of Physiology, Middlesex Hospital Medical School, London W1P 6DB (Received 7 December 1983) SUMMARY 1. The relationship ofplasma vasopressin concentrations in the physiological range to renal electrolyte excretion was investigated. 2. Unanaesthetized rats, when normally hydrated, were found to have a plasma vasopressin concentration of 113 + 015 ,su./ml. 16 h water deprivation raised this to 1P98+0-21 ,su./ml. 3. Inactin-anaesthetized rats infused with 0 45 % NaCl had a plasma vasopressin concentration of 1 19 + 0418 su./ml. Administration ofsynthetic arginine vasopressin at 6 and 24 ,uu./min raised plasma vasopressin levels to 1P88+0-17 and 4-26 + 0 43 ,uu./ml respectively. 4. In addition to the expected antidiuresis, vasopressin at a rate of 6 ,uu./min also produced a highly significant increase in Na+ excretion from 89 + 06 to 10-5+0-6/imol/min and Cl- excretion from 9-1+0-7 to 105+07j7mol/min. At 24 ,uu./min it produced larger increases in Na+ and Cl- excretion. 5. Inactin-anaesthetized hypophysectomized rats infused with 0 45 % NaCl had a plasma vasopressin concentration of only 017+004 #zu./ml. Administration of vasopressin at 6 and 24 #su./min raised plasma vasopressin levels in these animals to 0-63 + 0-17 and 2-20 + 0-11 su./ml respectively. 6. Hypophysectomized rats failed to exhibit a natriuresis in response to the lower dose of vasopressin, despite exhibiting an undiminished antidiuresis. The failure of the natriuresis may be related to the lower plasma vasopressin concentration achieved. 7. It is concluded that in the rat plasma vasopressin concentrations within the physiological range do influence Na+ and Cl- excretion by the kidney as well as controlling urine flow rate. INTRODUCTION The antidiuretic hormone, arginine vasopressin, is the major factor controlling the rate of urine flow in most mammalian species including the rat and human (Heller, R. J. Balment was a visiting lecturer to the University of Zimbabwe. Permanent address: Department of Zoology, University of Manchester, Manchester M13 9PL. 518 R. J. BALMENT AND OTHERS 1963). In addition to its antidiuretic effects, arginine vasopressin is known to have a natriuretic action (Jacobson & Kellog, 1956; Kurtzman, Rogers, Boonjarern & Arruda, 1975; Buckalew & Dimond, 1976). It is usually considered that a natriuretic response is seen only when supraphysiological levels of the hormone are present (Dicker, 1957; Atherton, Hai & Thomas, 1969; Kurtzman et al. 1975). In other studies, however, increases in electrolyte excretion have been observed in response to low rates ofadministration oflysine vasopressin (Atherton, Green & Thomas, 1971) and arginine vasopressin (Chan & du Vigneaud, 1970; Fejes-Toth & Szenasi, 1981); however, plasma vasopressin concentrations were not measured. Furthermore, Luke (1973) postulated that the natriuresis observed during hydropenia in the rat was due to vasopressin. An important role for vasopressin in the regulation of salt excretion in the sheep has also been suggested (Kinne, MacFarlane & Budtz-Olsen, 1961; Scott & Morton, 1976). In view of these conflicting opinions it seemed important to re-investigate the natriuretic effect of arginine vasopressin and to determine the plasma hormone level necessary to increase renal electrolyte excretion. Accordingly, plasma hormone concentrations and renal function have been assessed during infusions of synthetic arginine vasopressin. In the light of earlier reports (Buckalew & Dimond, 1976) of the involvement of other pituitary factors in the natriuretic response to vasopressin, these studies have been performed in hypophysectomized as well as in intact rats. METHODS Animak8 Experiments were performed on male Sprague-Dawley rats (320-460 g body weight) bred and housed in the Medical Faculty animal house at the University of Zimbabwe. Animals were maintained on a 12 h light/12 h dark regime and allowed free access to food (Mouse comproids, National Foods, Harare) and water. Renal8tudime Thirteen rats were anaesthetized with an intraperitoneal injection ofInactin (5-ethyl-5-(1'- methylpropyl)-2-thiobarbiturate; Byk Gulden) at 0-11 g/kg body weight. The right jugular vein was cannulated (Portex PP90). The urinary bladder was also cannulated (Portex PP90) via an incision in the abdominal wall (the dead space in the bladder cannula was approximately 150,ul). Body temperature was maintained at 37° 00 by means of a heated table. A further fifteen animals were treated in exactly the same way except that prior to cannulation their pituitaries were first exposed by the parapharyngeal approach, a dental drill (Shick HS2000/18) being used to drill through the base of the skull. The anterior and posterior lobes of the pituitary were then removed by suction, completeness of removal being checked post mortem. Both groups of animals were placed on a continuous jugular infusion of 0 45 % (0-077M) NaCl at 150 Fsl/min (Sage Syringe Pump model 351). An initial equilibration period of 4 h was allowed during which time urine was collected and its volume, Na+, K+ andCl- content measured. Following the equilibration period three consecutive urine collections were made into pre-weighed plastic vials atmin10 intervals. The infusate was then switched to one of identical ionic composition but containing synthetic arginine vasopression (Sigma grade V) at a concentration of either 40 or 160 Itu./ml, allowing delivery of the hormone to rats at 6 or 24 ,uu./min respectively (1 usu. equals approximately 2-5 pg). After a further three collectionsmin)(30 the animals were returned to the vasopressin-free infusate for the final six collectionsmin).(60 At the end of the experiment a 2 ml blood sample was taken by cardiac puncture, the plasma separated and assayed for Na+, K+ CCl.and VASOPRESSIN-INDUCED NATRIURESIS 519 Analytical methods Urine volume was determined gravimetrically. Urinary Na+ and K+ were determined by flame photometry (Corning model 435 flame photometer) and Cl- by conductivity meter (Corning 925 chloride analyser). Determination of plasma vasopressin concentrations (a) Follouing vasopre8sin administration. Parallel groups of 'intact' (n = 8) and 'hypophysecto- mized' (n = 6 or 7) were prepared and infused in the same way as the renal study groups. However, at the end of the 30 min period of vasopressin administration, at either 6 or 24 ,/u./min, the jugular cannula was clamped (to prevent contamination of the blood sample with infusate), the animals decapitated and trunk blood collected into pooled heparinized containers. All blood collections were completed within 30 s of stopping the infusion. Blood was also collected in a similar manner from control groups of 'intact' (n = 7) and 'hypophysectomized' (n = 5) rats which had received an infusion of 0 45 % NaCl for 5 h, but no vasopressin. Plasma was separated by centrifugation, and a 2 ml aliquot of each plasma sample was freeze-dried (Virtis Freeze-drier) and stored at -20 0C until dispatched by air to the Middlesex Hospital Medical School for determination of arginine vasopressin content by radioimmunoassay. The validity of this procedure for plasma storage and transport was verified by assay of vasopressin in plasma from hypophysectomized rats to which known concentrations (1 and 5 ,au./ml) of vasopressin had been added. (b) In unanaesthetized rats. Two groups of unanaesthetized rats were killed by decapitation and trunk blood collected, plasma separated and a known volume (1 or 2 ml) freeze-dried and assayed for arginine vasopressin. Rats in the first group (n = 12) were permitted free access to water up to the time ofdecapitation, while rats in the second group (n = 10) were deprived ofwater overnight (16 h). Assay of vasopressin Plasma samples were extracted with bentonite (Skowsky, Rosenbloom & Fisher, 1974) and then vasopressin concentrations determined by radioimmunoassay using radiolabelled (1261) vasopressin prepared with a solid phase lactoperoxidase method (Stromberg, Forsling & Akerlund, 1981). The results are presented in terms of the First International Standard for arginine vasopressin (77-501). There was no displacement of binding of labelled hormone in this assay by extracts of plasma from rats homozygous for congenital diabetes insipidus (Brattleboro strain). Statistical methods Values are presented as means + s.. of means. In the renal studies the mean excretory rate in the three control urine collections was used as a base line for comparison with subsequent collections, except where there was a progressive change through the control period as occurred for Na+ and Cl- excretion in hypophysectomized rats. In these latter cases the sloping base line was projected forwards for comparison with subsequent 10 min clearances (Balment, Brimble & Forsling, 1980). The significance of any deviations from the base line was assessed using a paired t test. All other comparisons of grouped data were by unpaired t test. RESULTS Fluid and electrolyte balance in 8udine-infused rats During the 4 h equilibration period the rats received 36 ml fluid and 2-77 mmol Na+ and C1- from the infusate. The total volume of urine produced and Na+, K+ and C1- excreted through this period is presented in Table 1. The amounts of water, Na+ and Cl- excreted were significantly less (P < 0 01) than the amounts infused both in intact and hypophysectomized animals. The hypophysectomized animals, however, excreted markedly less Na+ and Cl- (P < 0 01) than did intact rats, though the amount ofwater excreted was similar in both groups. The greater degree of salt retention in hypophysectomized animals extended into the experimental period (see Figs. 1 and 520 R. J. BALMENT AND OTHERS 2) and resulted in elevated plasma Na+ by comparison with intact rats (P < 0 01; Table 1).
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