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Experimental Physiology 89.5 pp 541-548
DOI: 10.1113/expphysiol.2004.027243
© The Physiological Society 2004
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Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats

F. V. Durlo1, M. Castro2, L. L. K. Elias3 and J. Antunes-Rodrigues3

1 Departamento de Patologia Clínica, Universidade de Campinas, UNICAMP, CEP 13083-970 Campinas, Sao Paulo, Brazil2 Departamento de Clínica Medica3 Departamento de Fisiologia, Faculdade de Medicina de Ribeirao Preto, USP, 14049-900 Ribeirao Preto, Sao Paulo, Brazil


   Abstract
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 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
The present study evaluated the effect of acute extracellular volume expansion (EVE) induced by intravenous injection of isotonic (0.15 M NaCl) or hypertonic saline (0.3 M NaCl) on prolactin, corticosterone, vasopressin, oxytocin and atrial natriuretic peptide (ANP) secretion. Male Wistar rats were treated with bromocriptine, sulpiride or dexamethasone. After isotonic and hypertonic EVE, the control group showed a significant increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increase in ANP and oxytocin levels in response to hypertonic EVE was more pronounced than to isotonic EVE. Bromocriptine and sulpiride treatments did not modify corticosterone, ANP and oxytocin responses to either isotonic or hypertonic EVE. The increases in prolactin and oxytocin, but not ANP, were blocked in dexamethasone pretreated rats. In conclusion, isotonic or hypertonic EVE induced an increase in the plasma concentrations of prolactin, corticosterone, ANP and oxytocin. The increases in ANP and oxytocin were independent of plasma concentrations of prolactin. The increases in prolactin and oxytocin were blocked by the inhibition of the hypothalamo–pituitary–adrenal (HPA) axis by dexamethasone. However, dexamethasone did not alter the increase in ANP secretion induced by isotonic or hypertonic EVE. Therefore, prolactin might participate in regulation of the hydroelectrolytic balance in mammals; however, in the present study, there was no evidence for direct interaction with ANPergic and oxytocinergic systems. In addition, the responses of prolactin and oxytocin induced by isotonic or hypertonic EVE are modulated by the HPA axis.

(Received 15 January 2004; accepted after revision 24 May 2004; first published online 7 June 2004)
Corresponding author M. Castro: Departamento de Clinica Medica, Faculdade de Medicina de Ribeirao Preto, USP, Avenue Bandeirantes 3900, 14049-900 Ribeirao Preto, Sao Paolo, Brazil. Email: castrom{at}fmrp.usp


   Introduction
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Atrial natriuretic peptide (ANP), described by De Bold et al. (1981), is mainly synthesized and released from atrial myocytes. As a potent vasodilator, ANP causes renal vasodilatation and increases the blood flow to the renal cortex, raising the glomerular filtration rate and reducing sodium and water reabsorption, thereby increasing diuresis and natriuresis. All of these actions promote a decrease in body fluid volume in response to the expansion of the extracellular volume (Gutkowska & Nemer, 1989; McCann et al. 1994). The main stimulus for ANP secretion is an increase in the transmural pressure of the atrial wall (Lang et al. 1985; Ellenbogen et al. 1988). Studies have demonstrated that the plasma concentration of ANP increases after extracellular volume expansion (EVE) induced by infusion of either isotonic or hypertonic solution (Pettersson et al. 1986; Antunes-Rodrigues et al. 1990, 1991, 1992; Elias et al. 1997; Maack, 1996). In addition to its effect on ANP release, we have shown that EVE induces oxytocin (OT) release, which plays an essential role in the regulation of the hydroelectrolytic balance (Haanwinckel et al. 1995). OT causes an increase in urinary osmolality, natriuresis, diuresis and kaliuresis, and inhibits sodium appetite (Antunes-Rodrigues et al. 1991; Blackburn et al. 1995).

Many studies have indicated that OT is involved in the regulation of prolactin (PRL) secretion in some physiological states. PRL is a pleiotropic hormone that influences multiple physiological mechanisms, including gonadotrophin secretion, development of the mammary glands, milk production and maintenance of milk secretion, immune system regulation, and cellular metabolism (Freeman et al. 2000). However, one of the least understood actions of PRL is its role in osmotic balance, regulating the transport of solutes and water across mammalian cell membranes (Shennan, 1994).

PRL has been shown to act on the proximal convoluted tubule of the renal nephron to promote sodium, potassium and water retention (Freeman et al. 2000). Rats treated with bromocriptine, a dopamine agonist that inhibits PRL synthesis and secretion (Ben-Jonathan, 1985), show a decrease in sodium and an increase in potassium transport across epithelial cells. (Bern, 1975; Falconer & Rowe, 1975). However, the role of PRL in osmotic balance differs among species. In fish and amphibians, PRL is very important for the maintenance of hydroelectrolytic balance. Studies have indicated that PRL might have an osmoregulatory function in mammalian embryos (Bern, 1975; Shennan, 1994), but the effect of PRL on the hydroelectrolytic balance in higher vertebrates has not been fully clarified. PRL has also been shown to be dramatically affected by different stress stimuli. A myriad of stressors have been used to characterize such effects on PRL secretion (Freeman et al. 2000). Under stress conditions, there is an adaptive response, including activation of the hypothalamo–pituitary–adrenal (HPA) axis (Dallman et al. 1992).

Since an interaction of PRL with ANP has been suggested (Gutkowska et al. 1997), we hypothesized that the effects of PRL on the hydroelectrolytic balance could be dependent on hormones, such as ANP or OT. Thus, in the present study we evaluated the effect of isotonic and hypertonic EVE on the secretion of PRL, ANP and OT in rats. For this purpose, we induced changes in PRL secretion using a dopamine receptor agonist or antagonist. We also evaluated the interplay between the HPA axis and PRL secretion in response to EVE.


   Methods
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Animals

This study was carried out in accordance with the guidelines of the Ethical Committee for animal use of School of Medicine of Ribeirao Preto, University of Sao Paulo. Adult male Wistar rats, weighing 180–200 g, were individually housed with controlled temperature (23–25°C), on a 12 h light–12 h dark cycle (lights on 07.00 h) with free access to rat chow and tap water. Experiments were conducted between 08.00 and 10.00 h. The animals were submitted to different experimental manipulations: a control group; a group treated with bromocriptine (0.4 mg (100 g body weight)–1I.P. in 200 µl, dissolved in 0.9% NaCl); a group treated with sulpiride, a dopamine receptor antagonist (1 g sulpiride (Equilid, Hoechst, Brazil) dissolved in 2 l of tap water (pH 7.5) and offered to the animals ad libitum, for 1 week); and a group treated with dexamethasone (Decadron, Prodome, Brazil; 100 µg (100 g body weight)–1S.C. in 200 µl, administered 2 h before the experiment).

Extracellular volume expansion

Twenty-four hours before the experiments, the animals were anaesthetized with 2,2,2-tribromoethanol (25 mg (100 g body weight)–1, Aldrich, Milwaukee, WI, USA) and a catheter was inserted into the right external jugular vein and advanced to the atrium (Harms & Ojeda, 1974). Blood volume expansion was performed in conscious, freely moving rats by I.V. injection of 0.15 or 0.3 M NaCl in a volume of 2 ml (100 g body weight)–1, over 1 min. The animals were killed by decapitation at different times (just before, 5, 10, 15 and 30 min after EVE) and blood samples were collected in tubes containing proteolytic enzyme inhibitors (2 mg EDTA, 20 µl of 500 µM phenylmethylsulphonyl fluoride and 20 µl of 500 µM pepstatin A) for the determination of plasma ANP, or heparin for the determination of PRL, OT and corticosterone.

Radioimmunoassays

Plasma PRL was determined in duplicate, using the NIDDK RIA reagents (NIH, Bethesda, MD, USA) and expressed in terms of the RP-1 reference preparations (Haanwinckel et al. 1991). Corticosterone was determined after ethanol extraction (Castro et al. 1995). ANP was measured after plasma extraction by activated octadecylsilane cartridge (SEP-COLUMN, Peninsula Laboratories, Belmont, CA, USA) as previously described (Gutkowska et al. 1984). OT was measured as previously reported (Haanwinckel et al. 1995). The assay sensitivity was 0.4 ng ml–1 for PRL, 0.4 µg dl–1 for corticosterone, 7.0 pg ml–1 for ANP and 0.9 pg ml–1 for OT. The inter- and intra-assay variations were, respectively, 11.7 and 5% for PRL, 8.4 and 5.7% for corticosterone, 11.7 and 6% for ANP, and 12.6 and 7% for OT.

Statistical analysis

All results are shown as means ±S.E.M. Differences between groups were assessed by Student's paired t test and analysis of variance (ANOVA). One-way ANOVA was used to compare baseline values and response to hypertonic and isotonic EVE. Two-way ANOVA was used to evaluate the response to hypertonic and isotonic EVE between different groups. ANOVA was followed by Newman–Keuls post hoc test. The level of significance was set at P < 0.05.


   Results
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Control group

Figure 1 shows plasma concentrations of PRL, corticosterone, ANP and OT under basal conditions and after isotonic EVE (I-EVE) or hypertonic EVE (H-EVE) in the control group. Plasma PRL levels showed similar and significant increases 5 min after I-EVE or H-EVE (P < 0.05) and returned by 15 min later to basal values. There was an increase in plasma corticosterone concentration after I-EVE or H-EVE at 5 min (P < 0.001), with a return to basal levels by 15 min after I-EVE, but not after H-EVE. There was an increase in the plasma concentration of ANP 5 min (P < 0.005) and 15 min (P < 0.01) after I-EVE or H-EVE. Plasma ANP levels were higher after H-EVE than after I-EVE at 5 min (P < 0.005). There was an increase in plasma concentrations of OT induced by I-EVE or H-EVE after 5 min (P= 0.001). Plasma OT levels were higher after H-EVE than after I-EVE at 5 min (P < 0.005) and 15 min (P < 0.005).



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  		Figure 1.  Effect of isotonic (I-EVE) or hypertonic (H-EVE) blood volume expansion on plasma PRL (ng ml–1), corticosterone (µg dl–1), ANP (pg ml–1) and OT (pg ml–1) concentrations in control animals (n= 8)
*P < 0.05versus basal; **P < 0.05 I-EVE versus H-EVE.

 
Bromocriptine-treated group

Figure 2 shows plasma concentrations of PRL, corticosterone, ANP and OT after I-EVE or H-EVE obtained in animals pretreated with bromocriptine. Rats treated with vehicle (control group) showed a significant increase in plasma levels of PRL after I-EVE (P= 0.01) or H-EVE (P < 0.005). In the bromocriptine-treated group there was no change in plasma PRL levels after I-EVE or H-EVE compared to the control basal levels. The bromocriptine-treated group showed lower PRL levels (P= 0.01) compared to the vehicle-treated group, both under basal conditions and in response to EVE. In vehicle and bromocriptine groups, corticosterone levels were not different in basal conditions and showed a similar increase at 5 min after I-EVE (P < 0.05) or H-EVE (P < 0.005), and these levels were sustained until 15 min. Plasma ANP and OT levels also showed an increase after I-EVE (P < 0.005) or H-EVE (P < 0.005) in both vehicle- and bromocriptine-treated groups. In both groups, plasma concentrations of both ANP and OT were higher after hypertonic compared to isotonic EVE (P= 0.01).



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  		Figure 2.  Effect of isotonic (I-EVE) or hypertonic (H-EVE) blood volume expansion on plasma PRL (ng ml–1), corticosterone (µg dl–1), ANP (pg ml–1) and OT (pg ml–1) concentrations in vehicle- or bromocriptine-treated animals (n= 6)
*P < 0.05versus basal; **P < 0.05 vehicle versus bromocriptine.

 
Sulpiride-treated group

Figure 3 shows plasma concentrations of PRL, corticosterone, ANP and OT after I-EVE or H-EVE obtained in animals pretreated with sulpiride. Plasma concentrations of PRL were significantly increased by I-EVE (P < 0.005) or H-EVE (P < 0.005) in the vehicle- and sulpiride-treated groups. The treatment with sulpiride induced a marked increase in PRL levels, in basal conditions as well as in response to I-EVE or H-EVE, compared to the group treated with vehicle at 5 and 15 min after extracellular volume expansion. Plasma concentrations of corticosterone in vehicle- and sulpiride-treated groups showed a similar increase 5 min after I-EVE (P < 0.05) or H-EVE (P < 0.05); however, these values were reduced 15 min after I-EVE, but not after H-EVE. Plasma concentrations of ANP and OT showed an increase after I-EVE and H-EVE in vehicle- and sulpiride-treated groups (P < 0.01). In both groups, plasma ANP and OT levels were higher after H-EVE than after I-EVE (P < 0.01).



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  		Figure 3.  Effect of isotonic (I-EVE) or hypertonic (H-EVE) blood volume expansion on plasma PRL (ng ml–1), corticosterone (µg dl–1), ANP (pg ml–1) and OT (pg ml–1) concentrations in vehicle- or sulpiride-treated animals (n= 6)
*P < 0.05versus basal; **P < 0.05 vehicle versus sulpiride.

 
Dexamethasone-treated group

Figure 4 shows plasma concentrations of PRL, corticosterone, ANP and OT after I-EVE or H-EVE in animals treated with dexamethasone. Plasma concentrations of PRL and corticosterone in the vehicle-treated group showed a significant increase at 5 min after I-EVE or H-EVE (P < 0.02); however, in the dexamethasone-treated group there were changes in neither PRL nor corticosterone after I-EVE or H-EVE. Plasma concentrations of ANP in vehicle- and dexamethasone-treated groups showed significant increases after I-EVE (P < 0.005) or H-EVE (P < 0.005); however, the increase observed after H-EVE was significantly greater than after I-EVE in both groups (P < 0.05). Plasma concentrations of OT in the vehicle-treated group showed a significant increase after I-EVE or H-EVE (P < 0.005); however, dexamethasone pretreatment significantly inhibited the increase in OT observed after both I-EVE and H-EVE.



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  		Figure 4.  Effect of isotonic (I-EVE) or hypertonic (H-EVE) blood volume expansion on plasma PRL (ng ml–1), corticosterone (µg dl–1), ANP (pg ml–1) and OT (pg ml–1) concentrations in vehicle- or dexamethasone-treated animals (n= 6)
*P < 0.05versus basal; **P < 0.05 vehicle versus dexamethasone.

 

   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Blood volume expansion induces several homeostatic responses to restore circulating volume through humoral and neural mechanisms. A significant increase in plasma ANP and OT after acute blood volume expansion caused by infusion of either isotonic or hypertonic solution has been demonstrated previously (Haanwinckel et al. 1995). In this study, we observed that ANP and OT levels were significantly higher after hypertonic EVE than after isotonic EVE. These results are in accordance with the participation of volume expansion and increased plasma osmolality as stimuli in the regulation of ANP release (Petersson et al. 1986; Antunes-Rodrigues et al. 1990, 1991, 1992; Elias et al. 1997; Ruskoaho, 1992). Therefore, the higher ANP secretion attained after hypertonic EVE in the present study may result from the simultaneous occurrence of the two stimuli (Haanwinckel et al. 1995). These results emphasize the importance of participation of ANP and OT in the hydroelectrolytic balance (Antunes-Rodrigues et al. 1991, 1993; Gutkowska et al. 1997; Soares et al. 1999). The mechanism of ANP action on hydroelectrolytic regulation involves water and sodium excretion, through a direct action on the kidneys and an indirect inhibition of aldosterone secretion by the adrenal cortex or inhibition of renin secretion by the juxtaglomerular cells in the kidneys (Atlas & Maack, 1987).

We have shown previously that EVE stimulates ANP release not only from the heart but also from the hypothalamus (Haanwinckel et al. 1995). In the present study, we confirmed previous data showing that EVE induces a concurrent OT and ANP release. Hypothalamic ANPergic neurones would induce OT release from the neurohypophysis that, in turn, would circulate to the heart where it would induce local ANP release (Favaretto et al. 1997; Petersson, 2002). This hypothesis is reinforced by the characterization of OT receptors in the rat heart that appear to be identical to those in other organs (Gutkowska et al. 2000; Jankowski et al. 2000; McCann et al. 2002).

In the present study, we also observed a significant increase in plasma PRL and corticosterone after EVE in control rats, suggesting that these hormones may also be involved in hydroelectrolytic regulation. Previous studies have shown an increase in plasma PRL induced by increased water and salt ingestion or after hypertonic EVE (Bliss & Lote, 1982). In order to evaluate the role of PRL in the regulation of ANP and OT secretion after isotonic or hypertonic EVE, we performed experiments using drugs that inhibit or stimulate PRL secretion. The results show that the ANP and OT responses to isotonic or hypertonic EVE did not differ between vehicle-, sulpiride- and bromocriptine-treated groups. These findings indicate that the ANP and OT responses to EVE are independent of PRL levels.

PRL, corticosterone and OT are hormones responsive to different forms of stress (Freeman et al. 2000). Indeed, OT and PRL have been found to increase after immobilization, hypoglycaemia and forced swimming (Lang et al. 1983). Hypothalamic factors, including serotonin, histamine, atrial natriuretic peptide and vasopressin, have been implicated in the stimulation of PRL secretion in response to different stressors (Freeman et al. 2000). In the present study, animals previously treated with dexamethasone showed no PRL response to isotonic or hypertonic EVE, suggesting that PRL release after EVE involves activation of the HPA axis. Indeed, the paraventricular nucleus of the hypothalamus has been shown to be important in PRL secretion, and may play a role in the suppression of tuberoinfundibular dopamine neurones (Freeman et al. 2000). Furthermore, the presence of corticotrophin-releasing hormone (CRH) receptors in these dopaminergic neurones has been demonstrated (Wong et al. 1994; Chen et al. 2000), suggesting a possible role of CRH in the regulation of PRL secretion.

We also found that the increase in plasma OT levels after isotonic or hypertonic EVE was blocked after inhibition of the HPA axis. This result agrees with a previous report that glucocorticoids exert an inhibitory effect on parvocellular OT-expressing neurones (Di et al. 2003). Thus, the present results suggest that the PRL and OT responses after EVE are likely to be modulated by HPA axis activity, as part of an integrative response to the stress induced by the manipulation of the rat or by EVE. However, dexamethasone did not modify the increase in ANP after EVE, indicating that ANP secretion induced by atrial stretching is not altered by glucocorticoids. The unchanged ANP secretion after EVE in rats pretreated with glucocorticoid indicates that dexamethasone, known to stimulate ANP release from the heart (Fink et al. 1992), may compensate for the reduced plasma concentrations of OT in this protocol.

In conclusion, PRL might participate in regulation of the hydroelectrolytic balance in mammals; however, there is no evidence for a direct interaction with ANPergic and oxytocinergic systems. In addition, the responses of the PRL and OT induced by isotonic or hypertonic EVE are modulated by the HPA axis.


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   Acknowledgements
 
The authors wish to thank Mrs Marina Holanda and Maria Valci Silva for technical assistance. We also thank Gareth Cuttle for the English revision. F.V.D. was supported by Fundacao de amparo pesquisa do Estado de Sao Paulo (FAPESP) (00/00066-1).




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