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Endocrinology Vol. 140, No. 6 2814-2818
Copyright © 1999 by The Endocrine Society

ARTICLES

Sodium Excretion and Renin Secretion after Continuous Versus Pulsatile Infusion of Oxytocin in Rats1

Mats Sjöquist, Wan Huang, Eva Jacobsson, Ole Skøtt, Edward M. Stricker and Alan F. Sved

Department of Physiology, Biomedical Center, Uppsala University (M.S., E.J.), Uppsala S-75123, Sweden; the Department of Physiology, University of Odense (O.S.), Odense DK-5000, Denmark; and the Department of Neuroscience, University of Pittsburgh (W.H., E.M.S., A.F.S.), Pittsburgh, Pennsylvania 15260 U.S.A.

Address all correspondence and requests for reprints to: Dr. Mats Sjöquist, Department of Physiology, Box 572, Biomedical Center, S-75123 Uppsala, Sweden. E-mail: mats.sjoquist{at}physiology.uu.se


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Neurohypophyseal oxytocin (OT), secreted continuously under conditions of hyperosmolality, is a potent natriuretic hormone in rats. In contrast, OT secretion during lactation is pulsatile and is not accompanied by increased urinary Na+ excretion. The present experiments compared the effects of continuous and pulsatile infusion of OT on natriuresis in rats. In male rats anesthetized with Inactin, continuous infusion of OT (125 ng/kg·h) increased plasma OT to about 70 pg/ml; renal Na+ excretion increased 10-fold, and urine volume and K+ excretion also were elevated. However, when OT was administered iv in the same amount but in pulses given once every 5 or 10 min, to simulate the pattern of OT secretion during lactation, rats did not excrete significantly more urine, Na+, or K+ than did vehicle-treated animals. The plasma renin concentration, measured in these experiments because OT receptors are present in the macula densa, increased 2-fold when OT was infused either continuously or in pulses. These results indicate that the effects of OT administration on urinary Na+ excretion in rats varies depending on whether the infusion is pulsatile or continuous, whereas the effects of OT on renin secretion show no such difference.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
IN CONSCIOUS rats, significant natriuresis results from the infusion of exogenous oxytocin (OT), in doses that increase plasma OT levels to within the physiological range (1, 2). A similar effect occurs when rats are water deprived or infused with hypertonic NaCl solution (3, 4), in response to which neurohypophyseal OT is secreted continuously. In contrast, increased urinary Na+ loss is not associated with lactation or parturition (5, 6) despite the large increases in OT secretion that are known to occur then (7, 8, 9, 10).

One difference between the increase in circulating OT levels that occurs in these various conditions is that pituitary OT secretion during lactation and parturition is intermittent rather than continuous (11, 12). Furthermore, the increased firing rate of hypothalamic oxytocinergic neurons during lactation and parturition also occurs in a pulsatile fashion, with an interval of 5–15 min between pulses of neuronal activity and OT release (7, 8, 9, 10, 13). This pattern of OT release results in acute increases in plasma OT levels that rapidly return to baseline before the subsequent pulse (9). Thus, it is plausible that natriuresis does not occur during lactation and parturition because the increase in plasma OT levels is pulsatile rather than steady.

The present studies were designed to test the hypothesis that natriuresis is not caused by pulsatile increases in plasma OT levels, produced experimentally to simulate the profile of plasma OT levels that occurs with lactation. The plasma renin concentration (PRC) was also measured in these studies because OT receptors in kidneys are present in the macula densa (14, 15, 16, 17, 18), which plays an important role in the stimulation of renin secretion (19).


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Animals
The experiments were performed on male Lewis x DA (F1 hybrids) rats, weighing 290–315 g. Female Lewis and male DA rats were purchased from ZFV (Hannover, Germany). Before the experiment, the animals had free access to tap water and a pelleted rat chow (R3, Ewos, Sodertalje, Sweden) containing 3 g Na+/kg, 8 g K+/kg, and 13 x 106 J/kg. All experiments were approved by the ethical committee for animal experiments of Uppsala.

On the day of the experiment, rats were anesthetized with Inactin (120 mg/kg, ip; Research Biochemicals International, Natick, MA) and placed on a servo-controlled heating pad to maintain rectal temperatures at 37.5 C. After tracheotomy, a femoral vein was cannulated for continuous infusion (5 ml/kg·h) of Ringer’s solution (129 mM NaCl, 2.5 mM KCl, 25 mM NaHCO3, and 0.75 mM CaCl2) to compensate for fluid losses during the experiment and for other iv treatments according to the protocols. A femoral artery was cannulated for blood sampling and monitoring arterial blood pressure. The urinary bladder was cannulated through a small abdominal incision for collection of urine samples. Experiments began 45 min after completion of the operative procedures.

Experimental protocols
Because the critical studies testing the hypothesis used Inactin-anesthetized rats, Exp 1 was performed to determine whether OT is a potent natriuretic hormone in this preparation, as it is in conscious rats (1, 2). After a 60-min control period during which all rats were infused with Ringer’s solution at the rate of 5 ml/kg·h, rats received for 80 min an iv infusion of OT at different rates: 0 (Ringer’s solution), 8, 25, 80, 250, 800, or 2500 ng/kg·h. Urine was collected in seven successive 20-min periods during the 140-min experimental period, for measurement of volume, Na+, K+, and osmolality. Blood samples were taken at the end of the period for measurement of plasma OT by RIA.

Exp 2 examined the effects of OT, administered iv in a continuous infusion or in pulsatile injections, on urinary Na+ excretion and renin secretion. Urine was collected during six successive periods of 20 min. After two control periods, OT was administered for 80 min in a dose of 125 ng/kg·h either as a continuous infusion or as 50-µl bolus injections at 1-, 5-, or 10-min intervals. A Y connector tube for injections was placed close to the insertion point of the venous catheter, so that the bolus injections of OT could occur simultaneously to the continuous infusion of vehicle. The total amounts of OT and administered volumes were calculated to be the same in all groups. A vehicle-treated group received only the Ringer’s solution.

At the end of experiments involving continuous infusion of OT, vehicle treatment, or bolus injection of OT at 10-min intervals, 2–3 ml blood were collected from the arterial line into ice-cold tubes containing 5% 0.1 M Na2 EDTA and centrifuged at 4 C and 1100 x g for 15 min. Plasma was withdrawn and stored at -70 C pending analysis of OT or PRC.

Analyses
In urine samples, the Na+ and K+ concentrations were assayed by flame photometry (IL 543, Instrumentation Laboratory, Milan, Italy), and osmolality was measured by freezing point depression (model 3MO, Advanced Instruments, Needham, MA).

OT was measured by RIA (20). Antiserum RI3 (Division of Neurophysiology and Neuropharmacology, Medical Research Council, London, UK), diluted 1:40,000, was used in the assay; the cross-reactivity of RI3 with vasopressin was 0.012%. All OT values included in this report were generated in a single assay; the assay sensitivity was 5 pg/ml, and the intraassay coefficient of variation was 8.4%. Recovery of OT from exogenously enriched plasma was 80.5%, and values were not corrected for this recovery.

PRC was measured by RIA of generated angiotensin I (21). Briefly, aliquots of plasma were diluted 20, 40, and 80 times with Tris(hydroxymethyl)aminomethane (Tris) buffer containing human albumin, and 5-µl portions of these samples were incubated for 24 h at 37 C with 20 µl of a reaction mixture that contained purified rat renin substrate (~1200 ng angiotensin I equivalents/ml). This incubation was followed by RIA of generated angiotensin I. Renin is expressed in Goldblatt units compared with renin standards (65/119) from the National Institute for Biological Standards and Control (Potters Bar, UK; 1 µGU = 160 pg angiotensin I/ml·h).

Statistical analysis
Results are presented as the mean ± SEM. Comparisons of groups were made by two-way ANOVA with repeated measures in the time parameter. Comparisons of OT levels and PRC between groups during the two last periods were made using Tukey’s highest significant difference test. P < 0.05 was considered statistically significant.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
Exp 1
The effects of logarithmically graded iv infusions of OT on renal Na+ excretion are shown in Fig. 1AGo. Urinary Na+ loss measured at the end of the 80-min infusion period increased in a dose-responsive manner. Significant natriuresis first occurred when the infusion rate was 25 ng/kg·h (P < 0.05), which produced a plasma OT concentration of about 26 pg/ml (Fig. 1BGo). Maximal natriuresis was achieved at a dosage of 250 ng/kg·h, which corresponded to a plasma OT level greater than 100 pg/ml (Fig. 1BGo).



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  		Figure 1. A, Sodium excretion (UNa) in control rats (0 dose) and in rats infused with OT in different doses, expressed as different infusion rates (nanograms per kg/h; n = 5 for all doses). All values are the mean ± SEM. B, The relationship between the OT dose and the measured plasma OT concentration. Plasma levels of OT expressed on a logarithmic scale corresponded linearly to the logarithmic values of different doses of OT infusion (r = 0.985; P < 0.0001; pOT = -25.7 - 3.87 x dose). An infusion of OT at the dose of 125 ng/kg·h used in Exp 2 would produce a plasma OT concentration of 71 pg/ml.

 
Exp 2
As shown in Fig. 2Go, rats that received vehicle infusion excreted only 0.2–0.4 µmol Na+/min in urine at a steady rate during the 80-min experimental period. In contrast, rats receiving a continuous iv infusion of OT at 125 ng/kg·h for 80 min showed a substantial, progressive increase in urinary Na+ excretion (P < 0.01). Injection of the same amount of OT delivered as a bolus of 2.08 ng/kg OT once each min for 80 min produced a response comparable to that of constant infusion, whereas urinary Na+ excretion in rats injected with OT as a bolus once every 5 or 10 min, with the dose again calculated to deliver 125 ng/kg·h, did not differ from that in control rats and was significantly less than the urinary Na+ excretion in rats infused continuously with OT.



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  		Figure 2. Mean (±SEM) Na excretion rate (UNa) before and during OT administration in five groups of rats: controls infused with vehicle solution (n = 6) and animals given continuous OT infusion (n = 6) or intermittent injections of OT at intervals of 1 min (n = 7), 5 min (n = 5), or 10 min (n = 6). Note that the administration of OT started after a 40-min baseline period during which vehicle solution was infused. *, P < 0.05; **, P < 0.01 (compared with the vehicle group).

 
Continuous OT infusion also produced a marked increase in urine flow (P < 0.01), which was similar to the diuresis observed when OT was administered as pulses delivered at 1-min intervals (Fig. 3Go). As with Na+ excretion, administration of OT with pulse intervals of 5 or 10 min produced less diuresis than continuous infusion of OT and was not significantly different from the urine flow observed in vehicle-treated control rats.



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  		Figure 3. Mean (±SEM) urine flow rate (Flow) before and during OT administration in five groups of rats: controls infused with vehicle solution (n = 6) and animals given continuous OT infusion (n = 6) or intermittent injections of OT at intervals of 1 min (n = 7), 5 min (n = 5), or 10 min (n = 6). Note that the administration of OT started after a 40-min baseline period during which vehicle solution was infused. *, P < 0.05; **, P < 0.01 (compared with the vehicle group).

 
Urinary K+ excretion was increased 3-fold by continuous OT infusion or OT injection at 1-min intervals (Table 1Go; both P < 0.01). In contrast, K+ excretion was not significantly altered by injection of OT at 5- or 10-min intervals. Urinary osmolarity was not significantly affected by any of the treatments and remained between 1600–2800 mosmol throughout the test period in all groups.


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  		Table 1. Mean ± SE of BP (arterial blood pressure), UK (urinary potassium excretion rate), and Osm (urine osmolality) in five groups at the end of the 40-min control period and the 80-min experimental period

 
In blood samples collected at the end of the 80-min test period, PRC was elevated 2-fold in rats receiving either bolus injections of OT given at 10-min intervals or a continuous infusion of OT (Fig. 4Go; both P < 0.05). Despite the increase in PRC, blood pressure was not significantly elevated in any group (Table 1Go).



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  		Figure 4. Mean (±SEM) PRC measured 80 min after OT was administered (125 ng/kg·h) either as intermittent injections of OT at 10-min intervals (n = 8) or as a continuous infusion (n = 11). Also presented are PRC after continuous infusion of Ringer’s solution as vehicle (n = 11). *, P < 0.05 compared with the vehicle group.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The principal finding of this study is that pulsatile increases in plasma OT levels did not elicit natriuresis in male rats. Thus, urinary Na+ did not increase when OT was administered as bolus injections at 5- or 10-min intervals, to simulate the pattern of OT release associated with lactation or parturition in female rats (7, 8, 9, 10). In contrast, marked natriuresis was observed when the same amount of OT was administered either with 1-min intervals between injections or as a continuous infusion in a dose that produced plasma OT levels of approximately 70 pg/ml.

The pattern of OT release during suckling has been well characterized in rats. Oxytocinergic neurons in paraventricular and supraoptic nuclei of the hypothalamus increase their firing rates for 2–4 sec at regular intervals of 5–15 min during suckling; each period of neurosecretory activity results in the release of about 1–3 ng OT from the posterior pituitary into the circulation. Blood samples collected within 30 sec of a suckling-induced burst of neurosecretory activity showed increases in plasma OT levels to 60–100 pg/ml, which declined quickly and had returned to control levels within 5 min (8, 9, 10). This time course of changes in plasma OT levels agrees well with that occurring after iv bolus injections of OT with 5- or 10-min intervals between injections (10). Nonetheless, this paradigm of OT administration does not result in natriuresis, which was observed during more continuous administration of the same amount of OT. Therefore, it appears that the OT receptors in mammary glands (and uterus) are sensitive to pulsatile exposure to OT, whereas the OT receptors mediating natriuresis require more continuous exposure to OT.

It is also possible that changes in OT receptor responsiveness during lactation or parturition may contribute to the lack of OT-induced natriuresis under these conditions. Estrogen treatment leads to an increase in renal OT receptor messenger RNA, as is also the case in the uterus and pituitary. However, at term the renal OT receptor messenger RNA decreased, whereas the levels in the uterus and pituitary increased (14, 22). Estrogen treatment increased the natriuretic effect of OT in ovariectomized rats (23). As male rats were the subjects in the current experiments, the effect of the pulsatile pattern on the renal actions of OT could not be accompanied by an influence of the female steroid hormones.

The dose-related natriuretic response to increases in plasma OT levels in Inactin-anesthetized rats was quantitatively similar to that observed in conscious rats (1, 2). In both Inactin-anesthetized rats and conscious male rats, the basal plasma OT concentration was approximately 10 pg/ml and increased to approximately 20 pg/ml under moderate hypernatremic conditions (3, 4). The apparent threshold for natriuresis of 15–26 pg/ml was much higher than was reported in a previous study (2), in part because rats in the earlier study (but not the present one) had been maintained on a low sodium diet to reduce basal urinary Na+ excretion and thereby make it easier to detect small increases in Na+ loss. Although in that study the suprathreshold effects of OT on urinary Na+ loss were linear, plasma OT levels achieved by iv infusion of OT did not exceed 70–90 pg/ml. A much larger range of doses was administered in the present experiment, and the results clearly indicate that further increases in natriuresis are not produced by very high, supraphysiological doses of OT that produce plasma OT levels above approximately 100 pg/ml. Thus, there is an apparent ceiling in the natriuretic effects of OT in rats.

The present study also examined the effect of iv OT on renin secretion, as renal OT receptors are present in the macula densa. Infusion of OT in rats significantly increased PRC. PRA was reported to increase when OT was infused into the vertebral artery of anesthetized dogs (24), but systemic OT levels were not measured in that experiment. The OT infusion associated with elevated PRC in the present experiment would be expected to increase plasma OT levels to 60–100 pg/ml based on the results of Exp 1. Because that level is similar to the response of rats to hypovolemia (25) and hypotension (26), it is possible that such changes in plasma OT levels contribute to the increase in PRC that is well known to occur when circulatory volume or pressure is reduced. Further experiments are needed to evaluate this hypothesis.

Interestingly, the increase in PRC observed in response to OT administration was similar regardless of whether OT was given by constant infusion or in a pulsatile fashion with 10-min intervals between injections. This observation stands in marked contrast to the different effects of those treatments on OT-induced natriuresis and suggests that OT-induced renin release is regulated independently of natriuresis. The increase in PRC associated with the pulsatile administration of OT suggests that increased PRC should be observed during lactation and parturition; in fact, PRC has been reported to increase in lactating rats (22).

In conclusion, OT administered iv to simulate the pulsatile pattern of pituitary OT release associated with lactation lacked the natriuretic action of continuously infused OT. Thus, the pulsatile pattern of OT release may protect against OT-induced loss of Na+ and fluid during suckling and parturition, which would be a sensible arrangement for rats under circumstances in which further fluid losses were best minimized. OT administration also increased PRC, regardless of whether OT was given by continuous infusion or in bolus injections. Thus, OT has multiple and independent effects on renal excretion and renin secretion, which have differing influences on Na+ and fluid homeostasis.


   Acknowledgments
 
We are grateful to Britta Isaksson and Mette Fredenslund for technical assistance, to Siu Lan Lee for conducting the OT assay, and to Dr. Per Melin (Ferring AB, Malmo, Sweden) for supplying the OT receptor antagonist.


   Footnotes
 
1 This work was funded by the Swedish Medical Research Council (Project 00140), the M. Bergvall Foundation, the T. & R. Söderberg Foundation, the Danish Health Sciences Research Council, the Novo Nordisk Foundation, and the U.S. NIMH (MH-25140). Back

Received November 2, 1998.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Conrad KP, Gellai M, North WG, Valtin H 1993 Influence of oxytocin on renal hemodynamics and sodium excretion. Ann NY Acad Sci 689:346–362[Abstract]
  2. Verbalis JG, Mangione MP, Stricker EM 1991 Oxytocin produces natriuresis in rats at physiological plasma concentrations. Endocrinology 128:1317–1322[Abstract]
  3. Huang W, Lee SL, Sjöquist M 1995 Natriuretic role of endogenous oxytocin in male rats infused with hypertonic NaCl. Am J Physiol 268:R634–R640
  4. Huang W, Lee SL, Arnason SS, Sjöquist M 1996 Dehydration natriuresis in male rats is mediated by oxytocin. Am J Physiol 270:R427–R433
  5. Arthur SK, Green R 1983 Renal function during lactation in the rat. J Physiol 334:379–393[Abstract/Free Full Text]
  6. Thiels E, Verbalis JG, Stricker EM 1990 Sodium appetite in lactating rats. Behav Neurosci 104:742–750[CrossRef][Medline]
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  8. Higuchi T, Tadokoro Y, Honda K, Negoro H 1986 Detailed analysis of blood oxytocin levels during suckling and parturition in the rat. J Endocrinol 110:251–256[Abstract]
  9. Lincoln DW, Wakerley JB 1975 Neurosecretory activation in the rat: correction of the suckling stimulus with the pulsatile release of oxytocin. J Physiol 245:42P–43P
  10. Meyer C, Freund MM, Guerne Y, Richard P 1987 Relationship between oxytocin release and amplitude of oxytocin cell neurosecretory bursts during suckling in the rat. J Endocrinol 114:263–270[Abstract]
  11. Brimble MJ, Dyball REJ 1977 Characterization of the responses of oxytocin- and vasopressin-secreting neurons in the supraoptic nucleus to osmotic stimulation. J Physiol 271:253–271[Abstract/Free Full Text]
  12. Brimble MJ, Dyball REJ, Forsling ML 1978 Oxytocin release following osmotic activation of oxytocin neurones in the paraventricular and supraotic nuclei. J Physiol 278:69–78[Abstract/Free Full Text]
  13. Boer K, Lincoln DW, Swaab DF 1975 Effects of electrical stimulation of the neurohypophysis on labour in the rat. J Endocrinol 65:163–176[Abstract]
  14. Breton C, Neculcea J, Zingg HH 1996 Renal oxytocin receptor messenger ribonucleic acid: characterization and regulation during pregnancy and in response to ovarian steroid treatment. Endocrinology 137:2711–2717[Abstract]
  15. Schmidt A, Jard S, Dreifuss JJ, Tribollet E 1990 Oxytocin receptors in rat kidney during development. Am J Physiol 259:F872–F881
  16. Stoeckel ME, Freund MM 1989 Autoradiographic demonstration of oxytocin-binding sites in the macula densa. Am J Physiol 257:F310–F314
  17. Tribollet E, Barberis C, Dreifuss JJ, Jard S 1988 Autoradiographic localization of vasopressin and oxytocin binding sites in rat kidney. Kidney Int 33:959–965[Medline]
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  19. Skøtt O, Briggs JP 1987 Direct demonstration of macula densa-mediated renin secretion. Science 237:1618–1620[Abstract/Free Full Text]
  20. Huang W, Lee SL, Sjöquist M 1994 Effects of neurohypophyseal antagonists in postnephrectomy natriuresis in male rats. Kidney Int 45:692–699[Medline]
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  23. Sjöquist M, Jacobsson E Estrogen modulation of the natriuretic effect of oxytocin in the rat. World Congress of Neurohypophyseal Hormones 1997, Montreal, Canada, p 112 (Abstract)
  24. Brooks DP, Share L, Crofton JT, Rockhold RW, Matsui K 1984 Effect of vertebral artery infusions of oxytocin on plasma vasopressin concentration, plasma renin activity, blood pressure and heart rate and their responses to hemorrhage. Neuroendocrinology 38:382–386[Medline]
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