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1 Laboratory of Neuroendocrinology, Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil
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(Received 22 March 2007;
accepted after revision 14 May 2007; first published online 18 May 2007)
Corresponding author J. Antunes-Rodrigues: Laboratory of Neuroendocrinology, Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Avenida Bandeirantes 3900, CEP: 14049–900, Ribeirao Preto, Sao Paulo, Brazil. Email: antunes{at}fmrp.usp.br
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Introduction |
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The magnocellular neurones of PVN and SON in the hypothalamus synthesize and release vasopressin (AVP) and oxytocin (OT; Bisset & Chowdrey, 1988; McKinley et al. 1999; Antunes-Rodrigues et al. 2004); in turn, OT in the systemic circulation can reach the cardiac atria and stimulate atrial natriuretic peptide (ANP) release (Haanwinckel et al. 1995; Gutkowska et al. 1997).
In rats, intracerebroventricular (I.C.V.) injection of NO donors has been shown to mediate the release of AVP (Ota et al. 1993; Yamaguchi et al. 2000), and the inhibition of NOS by N-nitro-L-arginine methyl ester (L-NAME) has been shown to decrease the release of AVP (Cao et al. 1996; Ventura et al. 2002). In contrast, other reports showed that I.C.V. injection of L-NAME induces an increase in plasma AVP and OT levels (Liu et al. 1997a; Kadekaro & Summy-Long, 2000). Furthermore, injection of L-NAME into the MnPO or SON produced an increase in urinary volume and sodium excretion (Saad et al. 2004a,b). These previous studies suggested that NO might play a physiological role in the regulation of AVP and OT release involved in the control of body fluid homeostasis.
The brain renin–angiotensin system plays an important role in the control of hydromineral balance and neuroendocrine secretion (Ferguson & Wall, 1992). In the rat brain, angiotensin II (Ang II) concentration increases in hypovolaemic conditions (Phillips et al. 1996; Saavedra, 2005) and it binds to angiotensin receptors, which are located in the CVOs, mainly in the SFO (Ferguson & Renaud, 1986; Lenkei et al. 1997). Injection of Ang II into the third or lateral ventricle or SFO, in rats, induces release of AVP, OT and ANP into the systemic circulation, as well as an increase in antidiuretic and natriuretic responses (Cunningham & Sawchenko, 1991; Bastos et al. 2001; Saad et al. 2002).
Double-labelling studies of the hypothalamic–neurohypophysial system have revealed that NOS is coexpressed with Ang II, AVP or OT (Calka & Block, 1993; Dawson et al. 1998; Xiao et al. 2005). These findings have led to speculation that NO participates in the modulation of AVP and OT secretion stimulated by Ang II. In fact, it has been demonstrated that the effects of I.C.V. administration of Ang II are enhanced by inhibition of the production of central NO, as observed by the enhancement of OT release, but not AVP release (Liu et al. 1997a; Kadekaro & Summy-Long, 2000).
Despite previous reports, there is controversy concerning the role of NO in the regulation of AVP secretion induced by different stimuli. Furthermore, the role of NO has usually been shown using an inhibitor of NOS (L-NAME) and its effects on AVP and OT secretion, but data using specific NO donors [3-morpholinylsydnoneimine chloride (SIN-1) or S-nitroso-N-acetyl penicillamine (SNAP)] associated with Ang II are scarce. Thus, in the present study, using an NOS inhibitor and NO donors, we investigated the role of the nitrergic system in the Ang II-induced changes in AVP, OT and ANP secretion and in urinary volume and sodium excretion.
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Methods |
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Male Wistar rats weighing 
260 g, obtained from the Central Animal Facility of the Campus of Ribeirao Preto, University of Sao Paulo, were kept in individual cages in an animal room with controlled temperature (23 ± 2°C) and a 12 h–12 h light–dark cycle (lights on between 06.00 and 18.00 h) with free access to food pellets and tap water. All experiments were conducted between 08.00 and 11.00 h. The experimental procedures were approved by the Ethical Committee for Animal Use of the School of Medicine of Ribeirao Preto, University of Sao Paulo (no. 038/2004).
Intracerebroventricular surgery
Each rat was anaesthetized with 2.5% tribromoethanol (Aldrich Chemical Co., USA; 1 ml (100 g body weight)–1, I.P.), placed in a stereotaxic instrument (Kopf, model 900), and the skull levelled between bregma and lambda. A stainless-steel guide cannula (10.0 mm long, 0.6 mm o.d., 0.4 mm i.d.) was unilaterally implanted into the right lateral cerebral ventricle (LV), based on the co-ordinates from the rat brain atlas of Paxinos & Watson (1997): 0.6 mm caudal to bregma, 1.5 mm lateral to the mid-line and 3.6 mm below the dura mater. The cannula was fixed to the cranium using dental acrylic resin and two jeweller's screws. A 30 gauge metal wire filled the cannula, except during the injections.
After surgery, the rats received a prophylactic injection of penicillin (50 000 U, I.M.) and were allowed to recover for 5–6 days, during which they were handled daily and habituated to the removal of the obturator of the guide cannula and to the gavage procedures, to minimize stress during the experimental phase. The correct placement of the I.C.V. cannula in the lateral ventricle was confirmed at the end of the experiment, after decapitation in unanaesthetized rats, by injection of Evans Blue (2% in 5 µl) into the intracerebroventricular system.
Experimental protocols
On the day of the experiment, all rats received two water loads (5% of body weight each, 37°C) by intragastric gavages at 60 min interval, with the purpose of increasing and producing a continuous urine flow. Immediately after the second water load, the animals were divided into two experimental protocols: protocol A, animals that received only I.C.V. injection of NOS inhibitor or NO donor; and protocol B: animals that received I.C.V. injection of NOS inhibitor or NO donor followed 20 min after by Ang II I.C.V. injection. The injections took 30–60 s each. For collection of urine samples, unanaesthetized freely moving rats were placed into individual metabolic cages without access to food and water. Complete voiding of urine was manually induced by gently pressing the suprapubic region of the animal at the end of the period. For measurement of hormonal plasma levels, the unanaesthatized animals were decapitated and the trunk blood was collected.
Protocol A: effects of central administration into the lateral ventricle of NOS inhibitor (L-NAME) or NO donors (SIN-1 or SNAP) on urinary parameters and hormone plasma levels in water-loaded rats Urinary volume, sodium and osmolality were measured. Isotonic saline (0.15 M NaCl in 5 µl, control group), L-NAME (250 µg in 5 µl), SIN-1 (10 µg in 5 µl) or SNAP (5 µg in 5 µl) was injected into the LV. After I.C.V. injection, urine samples were collected during a 60 min period. This protocol is related to the results presented in Fig. 1.
Plasma levels of AVP, OT and ANP were measured in another group of rats, which were subjected to the same protocol. Five minutes after I.C.V. injection, they were decapitated and the trunk blood was collected. This protocol is related to the results presented in Fig. 2.
Protocol B: effects of central administration into the lateral ventricle of NOS inhibitor (L-NAME) or NO donors (SIN-1 or SNAP) associated with injection of Ang II into the LV on urinary parameters and hormone plasma levels in water-loaded rats Urinary volume, sodium and osmolality were measured. Isotonic saline (0.15 M NaCl in 5 µl), L-NAME (250 µg in 5 µl), SIN-1 (10 µg in 5 µl) or SNAP (5 µg in 5 µl) was injected into the LV 20 min prior to the I.C.V. injection of Ang II (50 ng in 5 µl) or isotonic saline (5 µl). After I.C.V. injection of Ang II, urine samples were collected during a 60 min period. The control group comprised those rats that received the two injections of isotonic saline. This protocol is related to the results presented in Fig. 3.
Plasma levels of AVP, OT and ANP were measured in another group of rats subjected to the same protocol. Five minutes after I.C.V. injection of Ang II, they were decapitated and the trunk blood was collected. This protocol is related to the results presented in Fig. 4.
Drugs
The drugs were injected into the LV using a Hamilton microsyringe (10 µl) connected to a PE-10 polyethylene tube (25 cm), which was introduced into the guide cannula. The L-NAME (N-nitro-L-arginine methyl ester; 250 µg in 5 µl; 0.93 µmol) and Ang II (Asp-Arg-Val-Tyr-Lle-His-Pro-Phe; 50 ng in 5 µl; 48 pmol) were purchased from Sigma-Aldrich (St Louis, MO, USA) and dissolved in isotonic saline (0.15 M NaCl). The SIN-1 (3-morpholinylsydnoneimine chloride; 10 µg in 5 µl; 48 nmol) and SNAP (S-nitroso-N-acetyl penicillamine; 5 µg in 5 µl; 22.7 nmol) were purchased from Tocris (Ellisville, MO, USA) and dissolved in isotonic saline (0.15 M NaCl).
Determination of plasma levels of AVP, OT and ANP
Trunk blood was collected into cooled plastic tubes containing heparin (50 µl) for the measurement of AVP and OT. For the measurement of ANP, trunk blood was collected into cooled plastic tubes containing EDTA (2 mg ml–1 of blood) and proteolytic-enzyme inhibitors (20 µl of 1 mM phenylmethylsulphonyl fluoride and 20 µl of 500 µM pepstatin). Blood samples were centrifuged (1940g for 20 min at 4°C) and plasma was kept in a freezer at –20°C. For the AVP and OT determinations, samples were extracted from 1 ml of plasma with acetone and petroleum ether, and ANP was extracted from 1 ml of plasma using Sep-Pak C-18 cartridges (Waters Corporation, Milford, MA, USA). Plasma levels of AVP, OT and ANP were measured by specific radioimmunoassays as described by Elias et al. (1997), Haanwinckel et al. (1995) and Gutkowska et al. (1984), respectively. The lower limit of detection and intra- and interassay coefficients of variation were, respectively, 0.7 pmol l–1, 7.7% and 11.9% for AVP, 0.7 pmol l–1, 7.0% and 12.6% for OT, and 0.2 pmol l–1, 4.8% and 10.0% for ANP.
Measurements of urinary excretion
Urine samples were collected during a period of 60 min. Urinary volume was determined using 100 µl graduated tubes and expressed as microlitres per 100 grams body weight. Urinary sodium excretion was determined by flame photometer (Micronal, model b262) and expressed as millimoles per litre per 100 grams body weight. Urinary osmolality was measured by an osmometer (model 5004, Precision Systems, Natick, MA, USA), based on the freezing-point method and expressed as millimoles per kilogram H2O.
Statistical analyses
The results are reported as means ± S.E.M. In experimental protocol A, one-way ANOVA was followed by Student–Newman–Keuls post hoc multiple comparison test. In experimental protocol B, the data were analysed by two-way ANOVA followed by Student–Newman–Keuls post hoc test. Statistical analysis was performed using the SigmaStat program. Differences were considered significant at P < 0.05.
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Results |
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Urinary volume, sodium and osmolality (Fig. 1) One-way ANOVA showed significant differences in the values of urinary volume (F3,45 = 12.6, P < 0.001), sodium (F3,45 = 36.6, P < 0.001) and osmolality (F3,45 = 37.6, P < 0.001). Injection of L-NAME produced a reduction of urinary volume (P < 0.001) and an increase of urinary sodium (P < 0.001) and osmolality (P < 0.001) compared with the values observed in rats injected with isotonic saline. In contrast, injection of SIN-1 or SNAP did not change urinary volume, sodium or osmolality compared with the isotonic saline injection.
Plasma levels of AVP, OT and ANP (Fig. 2) One-way ANOVA showed significant differences in the plasma levels of AVP (F3,36 = 24.7, P < 0.001), OT (F3,36 = 45.9, P < 0.001) and ANP (F3,36 = 12.8, P < 0.001). Injection of L-NAME produced an increase in plasma levels of AVP (P < 0.001), OT (P < 0.001) and ANP (P < 0.001) compared with the injection of isotonic saline. Injections of SIN-1 or SNAP did not produce changes in plasma levels of AVP, OT or ANP compared with the isotonic saline injection.
Protocol B
Urinary volume, sodium and osmolality (Fig. 3) Two-way ANOVA showed significant differences in the values of urinary volume (F3,71 = 3.4, P < 0.05), sodium (F3,71 = 25.4, P < 0.001) and osmolality (F3,71 = 32.6, P < 0.001). Injection of L-NAME followed by I.C.V. injection of isotonic saline produced a reduction of urinary volume (P < 0.01) and an increase of urinary sodium (P < 0.05) and osmolality (P < 0.001) compared with the control group. Injection of Ang II in rats pretreated with isotonic saline reduced urinary volume (P < 0.001) compared with the control group, and this reduction was enhanced by L-NAME pretreatment (P < 0.01). In contrast, pretreatment with SIN-1 or SNAP blocked the antidiuretic effect of Ang II (P < 0.05 and P < 0.001, respectively). In addition, injection of Ang II in rats pretreated with isotonic saline produced an increase in urinary sodium (P < 0.001) and osmolality (P < 0.001) compared with the control group, and these responses were enhanced in L-NAME-pretreated rats (P < 0.001 and P < 0.001, respectively). In contrast, pretreatment with SIN-1 or SNAP blocked the natriuretic effect (P < 0.001 and P < 0.001, respectively) and the increase in urinary osmolality (P < 0.001 and P < 0.001, respectively) induced by Ang II.
Plasma levels of AVP, OT and ANP (Fig. 4) Two-way ANOVA showed significant differences in the plasma levels of AVP (F3,69 = 9.4, P < 0.001), OT (F3,69 = 3.9, P < 0.05) and ANP (F3,69 = 5.7, P < 0.01). Injection of L-NAME followed by I.C.V. injection of isotonic saline produced an increase in plasma levels of AVP (P < 0.001), OT (P < 0.01) and ANP (P < 0.001) compared with the control group. In rats pretreated with isotonic saline, the injection of Ang II produced an increase in plasma levels of AVP (P < 0.001), OT (P < 0.001) and ANP (P < 0.001) compared with the control group. In addition, in L-NAME-pretreated rats there was an enhancement of AVP, OT and ANP responses to Ang II (P < 0.001, P < 0.001 and P < 0.001, respectively). Conversely, pretreatment with SIN-1 blocked the increase in plasma levels of AVP (P < 0.001) and ANP (P < 0.05), while SNAP blocked the increase in plasma levels of AVP (P < 0.001), OT (P < 0.01) and ANP (P < 0.001) induced by Ang II.
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Discussion |
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Studies by Haanwinckel et al. (1995) and Gutkowska et al. (1997) demonstrated that intravenous injection of OT induces an increase in the plasma concentration of ANP with concomitant natriuresis, suggesting that OT participates in the control of ANP release by the heart. In the present study, it can be hypothesized that the increase in plasma levels of ANP induced by I.C.V. injection of L-NAME, with or without Ang II, may be a consequence of the released OT that travels via the systemic circulation to the cardiac atria and stimulates the release of ANP.
The role of NO in inhibiting AVP and OT release was previously reported in studies using in vitro isolated hypothalamus or neural lobes of rats, showing that L-NAME induces an increase in AVP and OT release (Lutz-Bucher & Koch, 1994), while NO donors reduce the release of these hormones induced by KCl (Yasin et al. 1993). Also, in hydrated rats, an increase in the plasma AVP and OT concentrations have been demonstrated after administration of L-NAME into the LV, suggesting that NO acts as an inhibitor of neurohypophysial hormone secretion (Kadekaro & Summy-Long, 2000).
The present data and the results described above emphasize the inhibitory action of NO on the secretion of neurohypophysial hormones. In the presence of a reduction of nitrergic tonus induced by L-NAME I.C.V. injection, there is a predominance of other pathways that stimulate AVP and OT release. However, we observed that the I.C.V. injection of NO donors (SIN-1 or SNAP) into the LV did not change the urinary volume, sodium or osmolality, or the plasma concentrations of AVP, OT and ANP in water-loaded rats. These data could suggest that, in these experimental conditions, the endogenous central nitrergic system may already be activated, and cannot be further enhanced by I.C.V. injection of NO donors.
The mechanism by which NO can inhibit AVP and OT release is not well established. One possibility is that NO acts as a conventional neurotransmissor (Zhang & Snyder, 1995) to counteract a component of the neural pathways involved in hormonal release. Experiments using in vitro and in vivo approaches demonstrated that L-NAME increased the discharge and NO donor inhibited the spontaneous electrical activity in SFO slices (Rauch et al. 1997; Li et al. 2005). It has also been shown that NO inhibits the firing activity of AVP and OT magnocellular neurones (Liu et al. 1997b; Ji & Mei, 2000; Stern & Ludwig, 2001). Alternatively, the neuroendocrine action of NO in the PVN and SON could be mediated by indirect actions, through local activation of a GABAergic inhibitory system (Zhang & Patel, 1998; Stern & Ludwig, 2001; Yang & Coote, 2003). Thus, NO can reach the presynaptic neurones in the circumventricular organs, where it decreases the release of neurotransmitters, e.g. Ang II (Bains & Ferguson, 1994), and directly or indirectly inhibits the postsynaptic activity of neurohypophysial neurones.
Reduction in blood volume or hypotension is a potent stimulus of AVP release (Bisset & Chowdrey, 1988; Thrasher, 1994). Therefore, the effects of NOS inhibitor and NO donors on blood pressure could also influence the neurohypophysial responses observed in the present study. However, it has been shown that I.C.V. injection of L-NAME produced an increase in blood pressure, while an NO donor did not induce changes in blood pressure (Liu et al. 1997a; Kadekaro & Summy-Long, 2000; Saad et al. 2004b). Thus, changes in blood pressure are unlikely to be involved in the control of AVP and OT changes observed in the present study.
It is well known that Ang II in the central nervous system acts as a neurotransmitter, involved in the control of renal water and sodium excretion and in secretion of AVP and OT in response to hypovolaemic conditions (Phillips et al. 1996; Antunes-Rodrigues et al. 2004). In addition, studies have demonstrated effects of Ang II, acting at the SFO, on the activity of neurohypophysial neurones and release of AVP and OT, which can be attenuated by SFO lesions (Ferguson & Renaud, 1986; Ferguson & Wall, 1992). In the present study, central angiotensinergic stimulation induced a reduction of urinary volume, followed by an increase in the natriuretic response and urinary osmolality, associated with an increase in the plasma levels of AVP, OT and ANP, confirming previous reports from Cunningham & Sawchenko (1991), Bastos et al. (2001) and Saad et al. (2002).
It has previously been observed that I.C.V. injection of L-NAME enhanced OT secretion in combination with Ang II or following haemorrhage (Liu et al. 1997a; Kadekaro et al. 1998; Kadekaro & Summy-Long, 2000). However, L-NAME was not able to amplify the increase in AVP levels in the same experimental conditions. Nevertheless, the present results show that pretreatment with L-NAME injected into the LV in rats subsequently stimulated with Ang II can increase the plasma levels not only of OT but also of AVP and ANP, with a concomitant increase in the antidiuretic and natriuretic effects, as well as the urinary osmolality. In addition, Giusti-Paiva et al. (2005) demonstrated that rats pretreated with L-NAME or SIN-1 and then subjected to endotoxic shock showed, respectively, an increase or decrease of the plasma levels of AVP and OT.
In an attempt to elucidate the controversial role of NO in the secretion of neurohypophysial hormones, in this study, besides the NOS inhibitor, we also used NO donors to verify the AVP and OT secretion induced by Ang II, associated with water and sodium excretion. Our data showed that pretreatment with NO donors blocked the increase in plasma levels of AVP, OT and ANP and the antidiuretic and natriuretic effects induced by Ang II. Therefore, taken together, the present results confirm the inhibitory action of the NO system on the Ang II effects on neurohypophysial secretion. Thus, it can be hypothesized that inhibition of the central nitrergic system facilitates angiotensinergic mechanisms, activating a direct or an indirect neural pathway that influences AVP and OT release and renal responses.
The administration of L-NAME and NO donors into the LV raises the possibility that these agents could diffuse throughout the ventricular system and reach the CVOs, MnPO and PVN (Li et al. 2006), crucial structures involved in the activation of neural pathways that regulate AVP and OT secretion. Rauch et al. (1997) demonstrated that an NO donor inhibits the electrical activity of SFO neurones stimulated by Ang II. Therefore, the inhibitory action of NO donors on the Ang II effects, observed in the present study, could be mediated by a direct effect on the CVOs and MnPO and, via their anatomical connections with PVN and SON (Johnson, 1985; Weiss & Hatton, 1990), could alter secretion of AVP and OT into plasma. Thus, the endogenous central nitrergic system could inhibit the action of Ang II in the SFO, decreasing neural inputs to the PVN and SON, and in this manner NO could modulate neurohypophysial hormone secretion.
Taken together, these results suggest that inhibition of the nitrergic system may act as a facilitatory mechanism, enhancing the effects on renal and hormonal responses induced by Ang II. In conclusion, these data suggest that nitric oxide can act as an inhibitory modulator of AVP and OT release, playing an important role in the control of body fluid homeostasis.
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