Utilization of steelmaking waste materials for production of calcium carbonate (CaCO3)

The steel industry produces, besides steel, also solid mineral by-products or slags, while it emits large quantities of carbon dioxide (CO2). Slags consist of various silicates and oxides which are formed in chemical reactions between the iron ore and the fluxing agents during the high temperature processing at the steel plant. Currently, these materials are recycled in the ironmaking processes, used as aggregates in construction, or landfilled as waste. The utilization rate of the steel slags can be increased by selectively extracting components from the mineral matrix. As an example, aqueous solutions of ammonium salts such as ammonium acetate, chloride and nitrate extract calcium quite selectively already at ambient temperature and pressure conditions. After the residual solids have been separated from the solution, calcium carbonate can be precipitated by feeding a CO2 flow through the solution. Precipitated calcium carbonate (PCC) is used in different applications as a filler material. Its largest consumer is the papermaking industry, which utilizes PCC because it enhances the optical properties of paper at a relatively low cost. Traditionally, PCC is manufactured from limestone, which is first calcined to calcium oxide, then slaked with water to calcium hydroxide and finally carbonated to PCC. This process emits large amounts of CO2, mainly because of the energy-intensive calcination step. This thesis presents research work on the scale-up of the above-mentioned ammonium salt based calcium extraction and carbonation method, named Slag2PCC. Extending the scope of the earlier studies, it is now shown that the parameters which mainly affect the calcium utilization efficiency are the solid-to-liquid ratio of steel slag and the ammonium salt solvent solution during extraction, the mean diameter of the slag particles, and the slag composition, especially the fractions of total calcium, silicon, vanadium and iron as well as the fraction of free calcium oxide. Regarding extraction kinetics, slag particle size, solid-to-liquid ratio and molar concentration of the solvent solution have the largest effect on the reaction rate. Solvent solution concentrations above 1 mol/L NH4Cl cause leaching of other elements besides calcium. Some of these such as iron and manganese result in solution coloring, which can be disadvantageous for the quality of the PCC product. Based on chemical composition analysis of the produced PCC samples, however, the product quality is mainly similar as in commercial products. Increasing the novelty of the work, other important parameters related to assessment of the PCC quality, such as particle size distribution and crystal morphology are studied as well. As in traditional PCC precipitation process, the ratio of calcium and carbonate ions controls the particle shape; a higher value for [Ca2+]/[CO32-] prefers precipitation of calcite polymorph, while vaterite forms when carbon species are present in excess. The third main polymorph, aragonite, is only formed at elevated temperatures, above 40-50 °C. In general, longer precipitation times cause transformation of vaterite to calcite or aragonite, but also result in particle agglomeration. The chemical equilibrium of ammonium and calcium ions and dissolved ammonia controlling the solution pH affects the particle sizes, too. Initial pH of 12-13 during the carbonation favors nonagglomerated particles with a diameter of 1 μm and smaller, while pH values of 9-10 generate more agglomerates of 10-20 μm. As a part of the research work, these findings are implemented in demonstrationscale experimental process setups. For the first time, the Slag2PCC technology is tested in scale of ~70 liters instead of laboratory scale only. Additionally, design of a setup of several hundreds of liters is discussed. For these purposes various process units such as inclined settlers and filters for solids separation, pumps and stirrers for material transfer and mixing as well as gas feeding equipment are dimensioned and developed. Overall emissions reduction of the current industrial processes and good product quality as the main targets, based on the performed partial life cycle assessment (LCA), it is most beneficial to utilize low concentration ammonium salt solutions for the Slag2PCC process. In this manner the post-treatment of the products does not require extensive use of washing and drying equipment, otherwise increasing the CO2 emissions of the process. The low solvent concentration Slag2PCC process causes negative CO2 emissions; thus, it can be seen as a carbon capture and utilization (CCU) method, which actually reduces the anthropogenic CO2 emissions compared to the alternative of not using the technology. Even if the amount of steel slag is too small for any substantial mitigation of global warming, the process can have both financial and environmental significance for individual steel manufacturers as a means to reduce the amounts of emitted CO2 and landfilled steel slag. Alternatively, it is possible to introduce the carbon dioxide directly into the mixture of steel slag and ammonium salt solution. The process would generate a 60-75% pure calcium carbonate mixture, the remaining 25-40% consisting of the residual steel slag. This calcium-rich material could be re-used in ironmaking as a fluxing agent instead of natural limestone. Even though this process option would require less process equipment compared to the Slag2PCC process, it still needs further studies regarding the practical usefulness of the products. Nevertheless, compared to several other CO2 emission reduction methods studied around the world, the within this thesis developed and studied processes have the advantage of existing markets for the produced materials, thus giving also a financial incentive for applying the technology in practice.

Correlations between ANP concentrations in atria, plasma and cerebral structures and sodium chloride preference in Wistar rats

We determined whether ANP (atrial natriuretic peptide) concentrations, measured by radioimmunoassay, in the ANPergic cerebral regions involved in regulation of sodium intake and excretion and pituitary gland correlated with differences in sodium preference among 40 Wistar male rats (180-220 g). Sodium preference was measured as mean spontaneous ingestion of 1.5% NaCl solution during a test period of 12 days. The relevant tissues included the olfactory bulb (OB), the posterior and anterior lobes of the pituitary gland (PP and AP, respectively), the median eminence (ME), the medial basal hypothalamus (MBH), and the region anteroventral to the third ventricle (AV3V). We also measured ANP content in the right (RA) and left atrium (LA) and plasma. The concentrations of ANP in the OB and the AP were correlated with sodium ingestion during the preceding 24 h, since an increase of ANP in these structures was associated with a reduced ingestion and vice-versa (OB: r = -0.3649, P<0.05; AP: r = -0.3291, P<0.05). Moreover, the AP exhibited a correlation between ANP concentration and mean NaCl intake (r = -0.4165, P<0.05), but this was not the case for the OB (r = 0.2422). This suggests that differences in sodium preference among individual male rats can be related to variations of AP ANP level. Earlier studies indicated that the OB is involved in the control of NaCl ingestion. Our data suggest that the OB ANP level may play a role mainly in day-to-day variations of sodium ingestion in the individual rat

Effect of metabolic acidosis on renal tubular sodium handling in rats as determined by lithium clearance

Systemic metabolic acidosis is known to cause a decrease in salt and water reabsorption by the kidney. We have used renal lithium clearance to investigate the effect of chronic, NH4Cl-induced metabolic acidosis on the renal handling of Na+ in male Wistar-Hannover rats (200-250 g). Chronic acidosis (pH 7.16 ± 0.13) caused a sustained increase in renal fractional Na+ excretion (267.9 ± 36.4%), accompanied by an increase in fractional proximal (113.3 ± 3.6%) and post-proximal (179.7 ± 20.2%) Na+ and urinary K+ (163.4 ± 5.6%) excretion when compared to control and pair-fed rats. These differences occurred in spite of an unchanged creatinine clearance and Na+ filtered load. A lower final body weight was observed in the acidotic (232 ± 4.6 g) and pair-fed (225 ± 3.6 g) rats compared to the controls (258 ± 3.7 g). In contrast, there was a significant increase in the kidney weights of acidotic rats (1.73 ± 0.05 g) compared to the other experimental groups (control, 1.46 ± 0.05 g; pair-fed, 1.4 ± 0.05 g). We suggest that altered renal Na+ and K+ handling in acidotic rats may result from a reciprocal relationship between the level of metabolism in renal tubules and ion transport.

Role of angiotensin II and vasopressin receptors within the supraoptic nucleus in water and sodium intake induced by the injection of angiotensin II into the medial septal area

In this study we investigated the effects of the injection into the supraoptic nucleus (SON) of non-peptide AT1- and AT2-angiotensin II (ANG II) receptor antagonists, DuP753 and PD123319, as well as of the arginine-vasopressin (AVP) receptor antagonist d(CH2)5-Tyr(Me)-AVP, on water and 3% NaCl intake induced by the injection of ANG II into the medial septal area (MSA). The effects on water or 3% NaCl intake were assessed in 30-h water-deprived or in 20-h water-deprived furosemide-treated adult male rats, respectively. The drugs were injected in 0.5 µl over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. Antagonists were injected at doses of 20, 80 and 180 nmol. Water and sodium intake was measured over a 2-h period. Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65%, N = 10, P<0.01) and sodium intake (81%, N = 8, P<0.01) induced by the injection of ANG II (10 nmol) into the MSA. Neither of these responses was significantly changed by injection of the AT2-receptor antagonist PD123319 into the SON. On the other hand, while there was a decrease in water intake (45%, N = 9, P<0.01), ANG II-induced sodium intake was significantly increased (70%, N = 8, P<0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Furthermore, they do not support the involvement of MSA AT2 receptors in the mediation of these responses.

The influence of septal lesions on sodium and water retention induced by Walker 256 tumor

In the course of studies on the effects of septal area lesions on neuroimmunomodulation and Walker 256 tumor development, it was observed that tumor-induced sodium and water retention was less marked in lesioned than in non-lesioned rats. In the present study possible mechanisms involved in this phenomenon were investigated. The experiments were performed in septal-lesioned (LW; N = 15) and sham-operated (SW; N = 7) 8-week-old male Wistar rats, which received multifocal simultaneous subcutaneous (sc) inoculations of Walker 256 tumor cells about 30 days after the stereotaxic surgery. Control groups (no tumor, sham-operated food-restricted (SFR), N = 7) and lesioned food-restricted (LFR, N = 10) were subjected to a feeding pattern similar to that observed in tumor-bearing animals. Multifocal inoculation of Walker 256 tumor rapidly induces anorexia, which is paradoxically accompanied by an increase in body weight, as a result of renal Na+ and fluid retention. These effects of the tumor were also seen in LW rats, although the rise in fractional sodium balance during the early clinical period was significantly smaller than in SW rats (day 4: SW = 47.6 ± 6.4% and LW = 13.8 ± 5.2%; day 5: SW = 57.5 ± 3.5% and LW = 25.7 ± 4.8%; day 6: SW = 54.4 ± 3.8% and LW = 32.1 ± 4.4%; P<0.05), suggesting a temporary reduction in tumor-induced sodium retention. In contrast, urine output was significantly reduced in SW rats and increased in LW rats (LW up to -0.85 and SW up to 4.5 ml/100 g body weight), with no change in osmolar excretion. These temporary changes in the tumor's effects on LW rats may reflect a "reversal" of the secondary central antidiuretic response induced by the tumor (from antidiuretic to diuretic).

Central lead administration inhibits water intake and sodium appetite in rats

We have demonstrated that acute third ventricle injections of lead acetate (PbAc) exert a powerful antidipsogenic effect and induce a significant increase in renal sodium excretion. In the present study we confirm the antidipsogenic effect of lead and demonstrate that central administration of this metal, in minute amounts, significantly reduces salt intake both during dehydration and after central angiotensinergic stimulation. Adult male Wistar rats had the third ventricle cannulated seven days before the experiments. During this period they had free access to distilled water and hypertonic saline solution (1.5%). After a 24-h period of fluid deprivation, experimental animals received third ventricle injections of PbAc (0.3, N = 8 and 3.0 nmol/rat, N = 14) while controls received sodium acetate (NaAc; 3.0 nmol/rat, N = 10). Rats treated with PbAc at the highest dose showed a significant reduction (P<0.05) both in water and hypertonic saline intake when compared to controls. When the effect of lead administration on angiotensin II-induced water and salt intake was studied, normohydrated animals received third ventricle injections of angiotensin II (9.6 nmol/rat) after pretreatment with 3.0 nmol/rat of PbAc (experimental group, N = 10) or NaAc (controls, N = 8). The group pretreated with PbAc presented a significant reduction (P<0.05) in both water and salt intake compared to controls. Thus, this study confirms the antidipsogenic effect of central lead injections and demonstrates that the presence of lead in the brain exerts a significant inhibition of sodium appetite.

Chromium mass balance in sodium chlorate process

Kuudenarvoista kromia käytetään natriumkloraatin valmistuksessa prosessin tuotantotehokkuuden ja turvallisuuden parantamiseksi. Kromia kuitenkin poistuu prosessista muutamaa reittiä pitkin. Koska kuuudenarvoisella kromilla on syöpää aiheuttavia, mutageenisiä sekä lisääntymiselle myrkyllisiä ominaisuuksia, olisi tärkeää ymmärtää, miten kromi kulkeutuu prosessin eri osiin, ja kuinka paljon sitä poistuu prosessista. Tämä on tärkeää, jotta osataan hallita kromin käytöstä aiheutuvat riskit, sekä toisaalta myös tehostaa kromin käyttöä prosessissa. Työn tarkoituksena oli tuottaa tietoa kromin käytöstä natriumkloraattiprosessissa. Työssä tutkittiin kromitasetta prosessin keskeisimmissä yksikköoperaatioissa. Myös kromin saostumista katodien pinnalle arvioitiin määrällisesti. Eri prosessinäytteistä tutkittiin lisäksi kromin hapetusasteita. Edellä mainittuja tutkimuskohteita varten määritettiin prosessinäytteiden kromipitoisuus. Eri prosessioperaatioille suoritettiin lisäksi taselaskelmat. Työn tuloksena esitettiin kromitase sekä yksikköoperaatioille että koko prosessille. Erinäisten epätarkkuustekijöiden vuoksi tasetta ei kuitenkaan pystytty määrittämään halutulla tarkkuudella, ja siksi työssä esitettyä tasetta voidaan pitää vain suuntaa antavana laskelmana. Katodien pinnalle saostunutta kromin määrää pidettiin kuitenkin oikean suuruusluokan tuloksena. Prosessinäytteiden hapetusasteita ei voitu arvioida, sillä saadut kokonaiskromitulokset eivät olleet täysin luotettavia. Huolimatta tulosten epätarkkuudesta, työ tuotti tärkeää tietoa prosessin toiminnasta kromin suhteen. Työtä voidaan hyödyntää jatkossa monin tavoin prosessin kromitaseen seurannassa.

Effect of inhibition of nitric oxide synthase on blood pressure and renal sodium handling in renal denervated rats

The role of sympathetic nerve activity in the changes in arterial blood pressure and renal function caused by the chronic administration of NG-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide (NO) synthesis, was examined in sham and bilaterally renal denervated rats. Several studies have demonstrated that sympathetic nerve activity is elevated acutely after L-NAME administration. To evaluate the role of renal nerve activity in L-NAME-induced hypertension, we compared the blood pressure response in four groups (N = 10 each) of male Wistar-Hannover rats weighing 200 to 250 g: 1) sham-operated vehicle-treated, 2) sham-operated L-NAME-treated, 3) denervated vehicle-treated, and 4) denervated L-NAME-treated rats. After renal denervation or sham surgery, one control week was followed by three weeks of oral administration of L-NAME by gavage. Arterial pressure was measured weekly in conscious rats by a tail-cuff method and renal function tests were performed in individual metabolic cages 0, 7, 14 and 21 days after the beginning of L-NAME administration. L-NAME (60 mg kg-1 day-1) progressively increased arterial pressure from 108 ± 6.0 to 149 ± 12 mmHg (P<0.05) in the sham-operated group by the third week of treatment which was accompanied by a fall in creatinine clearance from 336 ± 18 to 222 ± 59 µl min-1 100 g body weight-1 (P<0.05) and a rise in fractional urinary sodium excretion from 0.2 ± 0.04 to 1.62 ± 0.35% (P<0.05) and in sodium post-proximal fractional excretion from 0.54 ± 0.09 to 4.7 ± 0.86% (P<0.05). The development of hypertension was significantly delayed and attenuated in denervated L-NAME-treated rats. This was accompanied by a striking additional increase in fractional renal sodium and potassium excretion from 0.2 ± 0.04 to 4.5 ± 1.6% and from 0.1 ± 0.015 to 1.21 ± 0.37%, respectively, and an enhanced post-proximal sodium excretion compared to the sham-operated group. These differences occurred despite an unchanged creatinine clearance and Na+ filtered load. These results suggest that bilateral renal denervation delayed and attenuated the L-NAME-induced hypertension by promoting an additional decrease in tubule sodium reabsorption in the post-proximal segments of nephrons. Much of the hypertension caused by chronic NO synthesis inhibition is thus dependent on renal nerve activity.

Familial predisposition to hypertension and the association between urinary sodium excretion and blood pressure in a population-based sample of young adults

The reasons for the inconsistent association between salt consumption and blood pressure levels observed in within-society surveys are not known. A total of 157 normotensive subjects aged 18 to 35 years, selected at random in a cross-sectional population-based survey, answered a structured questionnaire. They were classified as strongly predisposed to hypertension when two or more first-degree relatives had a diagnosis of hypertension. Anthropometric parameters were obtained and sitting blood pressure was determined with aneroid sphygmomanometers. Sodium and potassium excretion was measured by flame spectrophotometry in an overnight urine sample. A positive correlation between blood pressure and urinary sodium excretion was detected only in the group of individuals strongly predisposed to hypertension, both for systolic blood pressure (r = 0.51, P<0.01) and diastolic blood pressure (r = 0.50, P<0.01). In a covariance analysis, after controlling for age, skin color and body mass index, individuals strongly predisposed to hypertension who excreted amounts of sodium above the median of the entire sample had higher systolic and diastolic blood pressure than subjects classified into the remaining conditions. The influence of familial predisposition to hypertension on the association between salt intake and blood pressure may be an additional explanation for the weak association between urinary sodium excretion and blood pressure observed in within-population studies, since it can influence the association between salt consumption and blood pressure in some but not all inhabitants.

Dietary sodium intake induced myenteric neuron hypertrophy in Wistar rats

In the present study we investigated the effect of salt intake on myenteric neuron size of the colon of adult male Wistar rats. The animals were placed on either a high-salt (HS; 8%; 12 animals) or a low-salt diet (LS; 0.15%; 12 animals) for 15 or 52 weeks and blood pressure was measured. The sizes of myenteric neurons of the distal colon from both groups were measured. No difference in neuron size was observed between the HS and LS groups after 15 weeks. After 52 weeks on HS, neuron size was increased (P<0.005) when compared with the LS group. The rats also presented hypertension, which was significantly different at 52 weeks (142 ± 11 vs 119 ± 7 mmHg). These results suggest that a long time on an HS diet can significantly increase myenteric nerve cell size.

Fighting by sleep-deprived rats as a possible manifestation of panic: effects of sodium lactate

Increased fighting is an effect of desynchronized sleep deprivation (DSD) in rats, and recently this behavior has been suggested to be spontaneous panic and equivalent to panic disorder. In the present study we tested this hypothesis by evaluating the effect of sodium lactate on this aggressiveness, because this substance is recognized to induce spontaneous panic attacks in patients. A total of 186 male albino Wistar rats, 250-350 g, 90-120 days of age, were submitted to DSD (multiple platform method) for 0, 4, or 5 days. At the end of the deprivation period the rats were divided into subgroups respectively injected intraperitoneally with 1.86, 2.98 and 3.72 g/kg of 1 M sodium lactate, or 1.86 and 3.72 g/kg of 2 M sodium lactate. The control animals were submitted to the same procedures but received equivalent injections of sodium chloride. Regardless of DSD time, sleep-deprived animals that received sodium lactate presented a significantly higher mean number of fights (0.13 ± 0.02 fights/min) and a longer mean time spent in confrontation (2.43 ± 0.66 s/min) than the controls (0.01 ± 0.006 fights/min and 0.12 ± 0.07 s/min, respectively; P<0.01, Student t-test). For the sodium lactate group, concentration of the solution and time of deprivation increased the number of fights, with the mean number of fights and mean duration of fighting episodes being greater with the 2.98 g/kg dose using 1 M lactate concentration. These results support the hypothesis that fighting induced by DSD is probably a spontaneous panic manifestation. However, additional investigations are necessary in order to accept this as a promising animal model for studies on panic disorder.

Effect of chronic oral administration of a low dose of captopril on sodium appetite of hypothyroid rats: Influence of aldosterone treatment

Rats rendered hypothyroid by treatment with methimazole develop an exaggerated sodium appetite. We investigated here the capacity of hypothyroid rats (N = 12 for each group) to respond to a low dose of captopril added to the ration, a paradigm which induces an increase in angiotensin II synthesis in cerebral areas that regulate sodium appetite by increasing the availability of circulating angiotensin I. In addition, we determined the influence of aldosterone in hypothyroid rats during the expression of spontaneous sodium appetite and after captopril treatment. Captopril significantly increased (P<0.05) the daily intake of 1.8% NaCl (in ml/100 g body weight) in hypothyroid rats after 36 days of methimazole administration (day 36: 9.2 ± 0.7 vs day 32: 2.8 ± 0.6 ml, on the 4th day after captopril treatment). After the discontinuation of captopril treatment, daily 1.8% NaCl intake reached values ranging from 10.0 ± 0.9 to 13.9 ± 1.0 ml, 48 to 60 days after treatment with methimazole. Aldosterone treatment significantly reduced (P<0.05) saline intake before (7.3 ± 1.6 vs day 0, 14.4 ± 1.3 ml) and after captopril treatment. Our results demonstrate that, although hypothyroid rats develop a deficiency in the production of all components of the renin-angiotensin-aldosterone system, their capacity to synthesize angiotensin II at the cerebral level is preserved. The partial reversal of daily 1.8% NaCl intake during aldosterone treatment suggests that sodium retention reduces both spontaneous and captopril-induced salt appetite.

Effect of sodium carboxymethylcellulose and methylprednisolone on the healing of jejunal anastomoses in rats

Sodium carboxymethylcellulose (SCMC) has been effective in reducing adhesion formation and corticosteroids reduce the inflammatory process. The objective of this study was to define the intraperitoneal (ip) effects of SCMC combined with intramuscular (im) methylprednisolone on peritoneal adhesion formation and on jejunal anastomosis healing in rats. Twenty Wistar rats (200-350 g) were divided into four groups (N = 5): groups I and III (controls) 5 and 21 days of treatment before sacrifice, respectively; groups II and IV (experimental groups) 5 and 21 days of treatment, respectively. SCMC (1%) was infused into the abdominal cavity and methylprednisolone (10 mg kg-1 day-1) was injected im daily from the day before surgery for animals of groups II and IV. All rats were submitted to a jejunal anastomosis. Sections of the anastomosis were prepared for routine histopathological analysis. The abdominal adhesion of group IV was less intense when compared with group III (P<0.0008). Anastomotic resistance was higher in groups II and IV when compared with groups I and III, respectively (P<0.05). There was no histological difference between groups I and II (exuberant granulation tissue on the serosal surface). Group III presented little peritoneal fibrinous tissue, with numerous thick collagen fibers. Group IV presented extensive although immature young fibrous tissue with rare thick collagen fibers. Sodium carboxymethylcellulose combined with corticosteroids seemed to diminish peritoneal adhesion but did not reduce anastomotic resistance.

Regulation of the renal proximal tubule second sodium pump by angiotensins

For several years it was believed that angiotensin II (Ang II) alone mediated the effects of the renin-angiotensin system. However, it has been observed that other peptides of this system, such as angiotensin-(1-7) (Ang-(1-7)), present biological activity. The effect of Ang II and Ang-(1-7) on renal sodium excretion has been associated, at least in part, with modulation of proximal tubule sodium reabsorption. In the present review, we discuss the evidence for the involvement of Na+-ATPase, called the second sodium pump, as a target for the actions of these compounds in the regulation of proximal tubule sodium reabsorption.

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity.