help button home button Endocrine Society JCEM
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Elias, L. L. K.
Right arrow Articles by Moreira, A. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Elias, L. L. K.
Right arrow Articles by Moreira, A. C.
The Journal of Clinical Endocrinology & Metabolism Vol. 82, No. 4 1243-1247
Copyright © 1997 by The Endocrine Society

Clinical Studies

Effect of Plasma Osmolality on Pituitary-Adrenal Responses to Corticotropin-Releasing Hormone and Atrial Natriuretic Peptide Changes in Central Diabetes Insipidus1

Lucila L. K. Elias, José Antunes-Rodrigues, Paula C. L. Elias and Ayrton C. Moreira

Endocrinology Division, Department of Medicine (L.L.K.E., P.C.L.E., A.C.M.); and Department of Physiology (J.A.R.), Faculty of Medicine, 14049–900, Ribeirão Preto, Brazil

Address all correspondence and requests for reprints to: Ayrton C. Moreira, Department of Medicine, Faculty of Medicine, 14049–900, Ribeirão Preto, SP, Brazil.


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
The objective of the present study was to examine the effect of changes in plasma osmolality (pOsm) on the responses of the pituitary-adrenal axis to CRH and atrial natriuretic peptide (ANP) release in patients with central diabetes insipidus (DI). Eight normal subjects and six DI patients were subjected to human CRH (hCRH) (1 µg/kg) stimulation alone or associated with isotonic volume loading (0.9% NaCl, 12 mL·kg·60 min) or an osmotic stimulus (5% NaCl, 0.06 mL·kg/min·120 min). The DI group showed significantly increased pOsm and undetectable or low plasma arginine vasopressin (AVP) during all tests. In the control group, pOsm and plasma AVP increased only during the osmotic stimulus. The DI group presented lower plasma ANP levels than controls during osmotic stimulus and isotonic volume loading. The lower ANP secretion in DI patients corroborates the importance of neurohypophyseal hormones in ANP regulation. Basal plasma ACTH and cortisol levels did not differ between controls and DI. The latter group presented a higher ACTH response than controls during stimulation with hCRH alone [area under the curve (AUC) 1138 ± 99 vs. 709 ± 62 pmol·L/min] and hCRH/5% NaCl (AUC 1602 ± 209 vs. 1158 ± 187 pmol·L·min). The DI cortisol AUC were higher than controls during stimulation with hCRH alone (65,471 ± 6,070 vs. 48,062 ± 3,476 nmol·L·min) and hCRH/5% NaCl (89,005 ± 10,043 vs. 62,105 ± 5,600 nmol·L·min). The highest ACTH and cortisol responses to hCRH in both groups were obtained with hCRH/5% NaCl. There was a significant correlation between mean pOsm and ACTH response to hCRH (r = 0.62). The increased responses to hCRH with increasing pOsm were present in control subjects and in patients with DI. However, at any given level of pOsm, there was no difference in ACTH response between controls and DI. These data indicate that the acute increases in pOsm augmented the ACTH and cortisol responses to hCRH that involve other factors besides magnocellular AVP.


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
ACTH RELEASE is mainly regulated by CRH (1, 2). It is well established that arginine vasopressin (AVP), colocalized with CRH in parvicellular neurons of the paraventricular nucleus of the hypothalamus, may act synergistically with CRH (3, 4, 5). Previous studies have demonstrated that high plasma osmolality (pOsm), a known stimulus of endogenous AVP release, increases ACTH and cortisol responses to CRH (6, 7, 8). Furthermore, genetically AVP-deficient rats have been reported to have subnormal pituitary-adrenal function (9, 10).

In addition to having a regulatory function on the anterior pituitary gland, AVP is present within the magnocellular neurons in the paraventricular and supraoptic nuclei of the hypothalamus projecting to the posterior pituitary, and is involved in water and salt homeostasis (11). The maintenance of fluid balance is achieved by the interaction of several systems besides AVP, such as the secretion of atrial natriuretic peptide (ANP). ANP was originally described in the cardiac atrium, and it was later demonstrated also in the brain, extending from the paraventricular nucleus to the anteroventral third ventricle region, a fact suggesting a role of ANP as a neuromodulator or neurotransmitter (12). There is evidence that ANP interacts with AVP inhibiting the volemic and osmotic release of AVP (13, 14, 15). On the other hand, the high ANP concentration described in the median eminence (16, 17) provided support for the reports that ANP may be a counterregulator of the hypothalamus-pituitary-adrenal axis (18, 19).

Therefore, in the present study we proposed to examine the interaction of pOsm, AVP, and ANP changes on pituitary-adrenal responses to human CRH during an osmotic stimulus and isotonic volume loading in control subjects and in patients with central diabetes insipidus (DI).


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Subjects and protocol

Eight normal subjects (two females and six males) aged 24–34 yr and six patients with DI (one female and five males) aged 20–46 yr were studied (Table 1Go) after obtaining informed consent and the approval of the Hospital Ethical Committee. The diagnosis of DI was established on the basis of the standard water deprivation test (20), and the patients had been treated with desmopressin that was stopped 36–48 h before the test. All patients but one had normal brain-pituitary computed tomography scans. Evaluation of the anterior pituitary was normal in all of them. The patients had free access to water until the beginning of the tests, but they were not allowed to drink during each test. Each subject was submitted to all of the following three tests in a randomized order: human CRH (hCRH) (Ferring Arzneimittel, GmbH, Kiel, Germany) alone (1 µg/kg iv), hCRH plus hypertonic saline (HS) (5% NaCl 0.06 mL·kg·min·120 min; hCRH/HS) and hCRH plus isotonic saline (IS) (0.9% NaCl, 12 mL·kg·60 min; hCRH/IS). The iv saline infusions were started 60 and 30 min before hCRH administration, respectively. Blood samples for plasma ACTH and cortisol measurements were collected 60 and 30 min before and 0, 15, 30, 45, 60, 90, and 120 min after hCRH administration. Serum sodium, AVP, ANP, and pOsm were determined every 30 min. All tests were started at 0900 h after an overnight fast and were separated by an interval of at least 7 days.


View this table:
[in this window]
[in a new window]
  		Table 1. Clinical and laboratory data on six patients with DI

 
Methods

Plasma ACTH and cortisol were determined by RIA after extraction with silicic acid (21) and ethanol (22), respectively. The assay sensitivity and intra-and interassay coefficients of variation (CV) were 3.4 pmol/L, 4.3% and 16% for ACTH and 30 nmol/L, 4.5% and 17% for cortisol. AVP and ANP were measured by RIA methods after extraction of plasma (1 mL and 2 mL, respectively) with acetone and petroleum ether (23) and an octadecasilyl silica cartridge (24). The percentages of recovery after extraction were 82% and 69%, respectively. AVP and ANP antiserum and 125I-ANP were purchased from Peninsula Laboratories (Belmont, CA) and 125I-AVP from Dupont (Dupont NEN Research Products, Boston, MA). The assay sensitivity and intra- and interassay coefficients of variation were 0.58 pmol/L, 2.7%, and 17% for AVP and 0.66 pmol/L, 4.8%, and 10% for ANP. All samples from an individual subject for all three tests were determined in duplicate in the same assay. Serum sodium was measured by flame photometry, and pOsm was determined by freezing point depression.

Statistical analysis

Data are expressed as mean ± SEM. For statistical purposes, AVP results that were below the detection limit of the assay were assigned as the half value of the detection limit. Basal levels were calculated as the mean of baseline values obtained in all three tests. The integrated ACTH and cortisol responses after hCRH were determined by calculating the area under the curve (AUC) from 15–120 min in relation to the CRH dose. Friedman’s ANOVA was performed for multiple comparisons. Wilcoxon’s paired rank test, the Wilcoxon Mann-Whitney test, and Spearman’s rank correlation were used when appropriate. Significance was assumed when P < 0.05.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The study was well tolerated. All subjects reported thirst elicited by HS infusion. Heart rate increased slightly 15–30 min after hCRH.

Effects of IS and HS infusion on pOsm, AVP, and ANP

Serum sodium did not change with IS infusion but rose (P < 0.05) from 139 ± 2.5 to 147 ± 2.6 mmol/L (controls) and from 143 ± 1.6 to 156 ± 1.4 mmol/L (DI) after HS.

In the control group, hematocrit fell significantly (P < 0.01) following both HS and IS infusions. On the other hand, the DI group presented an increase of hematocrit during the HS stimulus (P = 0.0005), and a nonsignificant decrease during IS infusion.

In the control group there were no pOsm or AVP changes during the hCRH and hCRH/IS tests; however, during the HS, pOsm and AVP increased (P < 0.0001) from 281 ± 1.5 to 300 ± 1.7 mOsm/kg and from 0.55 ± 0.1 pmol/L to 3.0 ± 0.8 pmol/L, respectively (Fig. 1Go). Basal pOsm did not differ between controls and DI. The latter group showed a significant increase in pOsm during the three tests, and the highest pOsm was obtained during the hCRH/HS test (P < 0.05). Plasma AVP remained undetectable or low during all tests in the DI group. AVP AUC was lower in the DI group than in controls during all tests.



View larger version (22K):
[in this window]
[in a new window]
  		Figure 1. Mean (± SEM) pOsm (upper), plasma AVP (middle), and ANP (lower) concentrations during stimulation with hCRH alone (1 µg/kg iv) ({circ}), hCRH plus 0.9% NaCl infusion ({blacksquare}), and hCRH plus 5% NaCl infusion ({blacktriangleup}) in eight control subjects and six patients with DI.

 
The mean basal plasma ANP was lower in the DI group than in controls (5.6 ± 0.6 vs. 9.5 ± 0.8 pmol/L) (P < 0.005) (Fig. 1Go). IS and HS infusions elicited ANP secretion in both groups (P < 0.003). Plasma ANP levels during HS were higher than during the IS loading in controls (AUC 2035 ± 258 vs. 2664 ± 268 pmol/L) and DI (AUC 1205 ± 167 vs. 1799 ± 256 pmol/L min) (P < 0.05). The DI group presented lower plasma ANP levels than controls during HS and IS infusions.

Responses of plasma ACTH and cortisol to hCRH

There was no difference between control and DI basal ACTH levels (5.8 ± 0.6 vs. 6.2 ± 0.5 pmol/L) (Fig. 2Go). The ACTH peak was higher with hCRH/HS in both groups (P < 0.05) (Table 2Go). The DI group presented a higher ACTH peak than the control only after hCRH alone (P < 0.02). The plasma ACTH AUC for the control group did not differ in the hCRH and hCRH/IS tests, but the values of both tests were lower (P < 0.02) than the values of the hCRH/HS test (Fig. 3Go). The DI group also showed a higher ACTH AUC with hCRH/HS when compared with the other two tests (P < 0.03). In this group the integrated ACTH response to hCRH/IS was lower than to hCRH alone (P < 0.03). The ACTH AUC was higher in the DI group than in the control during the hCRH (P < 0.005).



View larger version (29K):
[in this window]
[in a new window]
  		Figure 2. Mean (± SEM) plasma ACTH (lower) and cortisol (upper) concentration responses to hCRH alone (1 µg/kg iv) given at time 0 ({circ}), hCRH plus 0.9% NaCl infusion (12 mL·kg·60 min) ({blacksquare}), and hCRH plus 5% NaCl infusion (0.06 mL·kg·min·120 min) ({blacktriangleup}) in eight control subjects and six patients with DI.

 

View this table:
[in this window]
[in a new window]
  		Table 2. Mean (± SEM) plasma ACTH (pmol/L) and cortisol (nmol/L) levels under baseline conditions and during 0.9% and 5% NaCl infusion before hCRH (time 0) and their peak responses after hCRH in control subjects and DI patients

 


View larger version (17K):
[in this window]
[in a new window]
  		Figure 3. Mean (± SEM) AUC for ACTH and cortisol response to hCRH alone, hCRH plus 0.9% NaCl infusion, and hCRH plus 5% NaCl infusion in eight control subjects and six patients DI. *, P < 0.05 compared with other two tests within group; **. P < 0.05 compared with control group; ***. P = 0.05 < P < 0.1 compared with control group.

 
The mean basal cortisol levels obtained in the three tests did not differ between controls and DI group. In the control group the IS and HS infusions did not change the basal cortisol level (Fig. 2Go). There was also no change in basal cortisol level with IS in the DI group, but HS infusion increased the basal cortisol level from 392 ± 33 to 593 ± 74 nmol/L (Table 2Go). The cortisol peak after hCRH/HS was higher than after the other two tests in both groups and did not differ between controls and DI patients. The cortisol AUC was higher during the hCRH/HS test than during the other two tests in both the control and DI groups. The DI cortisol AUC was higher than control during the hCRH and hCRH/HS tests (Fig. 3Go).

A significant positive correlation was observed between mean pOsm and plasma ACTH AUC responses to hCRH in all subjects as a whole during the three tests (r = 0.62 n = 41; P < 0.0001; Fig. 4Go).



View larger version (22K):
[in this window]
[in a new window]
  		Figure 4. Correlation between AUC for plasma ACTH response and mean pOsm obtained with hCRH alone, hCRH plus 0.9% NaCl infusion, and hCRH plus 5% NaCl infusion in control subjects (open symbols) and patients with DI (black symbols).

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
AVP has been shown to act as an ACTH secretagog potentiating the CRH effect in humans both after exogenous administration (4, 5) and after an endogenous secretion (6, 7, 8). The present data show that in control subjects the increase in pOsm was associated with an increased ACTH and cortisol response to hCRH. This feature agrees with previous reports that hypertonic saline infusion not only stimulates basal ACTH and cortisol secretion, but also augments the hormonal responses to CRH in normal individuals (6, 7). These investigators suggested that the greater response following HS was related to endogenous AVP secretion associated with the rise in pOsm. However, in the present study the DI patients showed a higher response to hCRH alone than controls. These results are similar to those reported by Mazza and colleagues (25), who also showed an exaggerated pituitary-adrenal response to hCRH in DI patients. In addition, the present study originally demonstrates that DI patients also presented increased ACTH and cortisol responses to hCRH associated with the osmotic stimulus. The DI patients were studied without desmopressin, and they were not allowed to drink during each test. Thus, they achieved higher pOsm than controls even during the test with hCRH alone, with consequent higher ACTH and cortisol responses than controls. Furthermore, we obtained a positive correlation between pOsm and hCRH-induced ACTH secretion in all subjects as a whole with the three tests. Thus, the increased response to hCRH with increasing pOsm was presented under normal conditions and was augmented in DI, probably because of the higher pOsm attained by this group, indicating that an acute increase of pOsm may participate in pituitary-adrenal regulation. However, at any given level of pOsm, there was no difference in ACTH response between controls and DI patients. Therefore, the increased ACTH response to hCRH with the increase of pOsm may be independent of magnocellular AVP, suggesting other possible mechanisms involved in the ACTH-osmoregulation interaction. Parvicellular AVP secretion may be preserved in DI patients (26) and may contribute to those responses. Additionally, we cannot rule out an increased sensitivity to the administered hCRH in DI, because AVP seems to contribute to the down-regulation of pituitary CRH receptors (27).

In addition, we should take into account the secretion of other factors stimulated by the increased pOsm that may compensate for the lack of AVP. Plasma oxytocin concentration is elevated and positively correlated with pOsm in the Brattleboro rat (28). However, oxytocin has been reported not to be involved in osmoregulation in man (29, 30). Angiotensin II stimulates ACTH release and potentiates the effects of CRH (31). Patients with DI are hyperreninemic both under basal and water-deprivation conditions (32). We then postulated that an exaggerated activation of the central angiotensin II system may contribute to the higher hCRH responses obtained for our DI patients.

The present study also indicates that the hydration status of DI patients may contribute to the enhanced response to hCRH, because IS infusion resulted in a similar response to hCRH in DI and control subjects. Furthermore, at the beginning of each test when pOsm was similar for DI and control subjects, plasma ACTH and cortisol concentrations were normal.

Our results also showed that in controls ANP secretion was elicited by IS loading and was higher during HS infusion. These data are in accordance with the participation of both stimuli of volume expansion and increased pOsm in the regulation of ANP release (33). The augmented ANP secretion attained during HS infusion in controls may result from the simultaneous occurrence of the two stimuli. The ANP concentrations attained in the DI group with HS infusion compared with IS infusion in the presence of a decrease of plasma volume suggests that plasma tonicity per se could mediate ANP release. The present study also originally demonstrated that stimulated ANP secretion was lower in DI patients than in controls. Our results extend a previous report showing that DI patients have lower baseline plasma ANP levels (34). The lower ANP secretion in DI patients than controls corroborates the importance of neurohypophyseal hormones in regulating ANP secretion (35, 36).

ANP has been described as a possible inhibitor of ACTH secretion (18, 19). In DI patients the lower ANP release may reduce the inhibition of ACTH secretion, contributing to their greater ACTH and cortisol responses to hCRH.

In conclusion, the DI patients showed an enhanced ACTH-cortisol responses to hCRH alone and to hCRH associated with an osmotic stimulus. There is a positive correlation between pOsm and ACTH release. These findings suggest that an acute increase of pOsm may participate in pituitary-adrenal regulation involving other factors besides magnocellular AVP.


   Acknowledgments
 
The authors thank Miss Adriana Rossi, Miss Lucimara Bueno, Mr. J. Roberto Silva, Mr. Odair Araújo, Mr. Baltazar Nunes, and Mrs. Ines Araújo for technical assistance. We also thank Dr. S.M. McCann for critical review of the manuscript and Mrs. E. Greene for revision of the English text. Reagents for ACTH RIA were supplied by the National Hormone and Pituitary Program, NIDDK, Baltimore, MD.


   Footnotes
 
1 This work was supported by Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq Grant 521595/94–0) and Hospital das Clínicas de Ribeirão Preto (HCFMRP-FAEPA). Back

Received July 19, 1996.

Revised December 27, 1996.

Accepted January 9, 1997.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

  1. Vale W, Spiess J, Rivier C, Rivier J. 1981 Characterization of a 41-residue ovine hypothalamic peptide that stimulates secretion of corticotropin and ß-endorphin. Science. 213:1394–1397.[Free Full Text]
  2. Jones MT, Gillham B. 1988 Factors involved in the regulation of adrenocorticotropic hormone/ß-lipotropic hormone. Physiol Rev. 68:743–818.[Free Full Text]
  3. Gillies GE, Linton EA, Lowry PJ. 1982 Corticotropin releasing activity of the new CRF is potentiated several times by vasopressin. Nature. 299:355–357.[CrossRef][Medline]
  4. Debold CR, Sheldon WR, Decherney GS, et al. 1984 Arginine vasopressin potentiates adrenocorticotropin release induced by ovine corticotropin-releasing factor. J Clin Invest. 73:533–538.
  5. Arai K, Takebe K. 1991 Corticotropin response to combined administration of human corticotropin-releasing hormone and small-dose arginine vasopressin in normal, subjects. Metabolism. 40:1088–1091.[CrossRef][Medline]
  6. Milsom RS, Conaglen JV, Donald RA, Espiner EA, Nicholls MG, Livesey JH. 1985 Augmentation of the response to the CRF in man: relative contributions of endogenous angiotensin and vasopressin. Clin Endocrinol (Oxf). 22:623–628.[Medline]
  7. Rittmaster RS, Cutler, Jr, GB, Gold PW, et al. 1987 The relationship of saline-induced changes in vasopressin secretion to basal and corticotropin-releasing hormone-stimulated adrenocorticotropin and cortisol secretion in man. J Clin Endocrinol Metab. 64:371–376.[Abstract]
  8. Watabe T, Tanaka K, Kumagae M, et al. 1988 Role of endogenous arginine vasopressin in potentiating corticotropin-releasing hormone-stimulated corticotropin secretion in man. J Clin Endocrinol Metab. 66:1132–1137.[Abstract]
  9. McCann SM, Antunes-Rodrigues J, Nallar R, Valtin H. 1966 Pituitary-adrenal function in the absence of vasopressin. Endocrinology. 79:1958–1064.
  10. Buckingham JC, Leach JH. 1980 Hypothalamo-pituitary-adrenocortical function in rats with inherited diabetes insipidus. J Physiol. 305:397–404.[Abstract/Free Full Text]
  11. Bisset GW, Chowrey HS. 1988 Control of release of vasopressin by neuroendocrine reflexes. Q J Exp Physiol. 73:811–872.[Free Full Text]
  12. Imura H, Nakao K, Itoh H. 1992 The natriuretic peptide system in the brain: implications in the central control of cardiovascular and neuroendocrine functions. Front Neuroendocrinol. 13:217–249.[Medline]
  13. Samson WK. 1985 Atrial natriuretic factor inhibits dehydration and hemorrhage-induced vasopressin release. Neuroendocrinology. 40:277–279.[CrossRef][Medline]
  14. Clark BA, Elahi D, Fish L, et al. 1991 Atrial natriuretic peptide suppresses osmostimulated vasopressin release in young and elderly humans. Am J Physiol. 261:E252–E256.
  15. Thrasher TN, Ramsay DJ. 1993 Interactions between vasopressin and atrial natriuretic peptides. Ann NY Acad Sci. 689:426–437.[CrossRef][Medline]
  16. Palkovits M, Eskay RL, Antoni FA. 1987 Atrial natriuretic peptide in the median eminence is of paraventricular nucleus origin. Neuroendocrinology. 46:542–544.[Medline]
  17. Lim AT, Sheward WJ, Copolov D, Windmill D, Fink G. 1990 Atrial natriuretic factor is released into hypophysial portal blood: direct evidence that atrial natriuretic factor may be a neurohormone involved in hypothalamic pituitary control. J Neuroendocrinol. 2:15–18.[CrossRef]
  18. Dayanithi G, Antoni FA. 1989 Atriopeptins are potent inhibitors of ACTH secretion by rat anterior pituitary cells in vitro: involvement of the atrial natriuretic factor receptor domain of membrane-bound guanylyl cyclase. J Endocrinol. 125:39–44.
  19. Franci CR, Anselmo-Franci JA, McCann SM. 1992 The role of endogenous atrial natriuretic peptide in resting and stress-induced release of corticotropin, prolactin, growth hormone, and thyroid-stimulating hormone. Proc Natl Acad Sci USA. 89:11391–11395.[Abstract/Free Full Text]
  20. Miller M, Dalakos T, Moses AM, Fellerman H. Streeten DHP. 1970 Recognition of partial defects in antidiuretic hormone secretion. Ann Int Med. 73:721–729.
  21. Moreira AC, Barizon EA, Silva JR. 1987 Standardization of a radioimmunoassay for plasma ACTH. Arq Bras Endocrinol Metab. 31:19–22.
  22. Vieira JGH. 1977 Radioimmunoassay of serum cortisol. MA thesis. São Paulo: Escola Paulista de Medicina; 1–67.
  23. Glick SM, Kagan A. 1979 Vasopressin. In: Jaffe BM, Behrman HR, (eds) Methods of Hormone Radioimmunoassay, ed 2. New York: Academic Press; 341–351.
  24. Gutkowska J, Horky K, Thibault G, Januszewicz P, Cantin M, Genest J. 1984 Atrial natriuretic factor is a circulating hormone. Biochem Biophys Res Commun. 30:315–323.
  25. Mazza E, Goffi S, Barchi P, et al. 1994 Enhanced adrenocorticotrophic hormone and cortisol responses to corticotrophin-releasing hormone in central diabetes insipidus. Eur J Endocrinol. 130:121–124.[Abstract/Free Full Text]
  26. Green JR, Buchan GC, Alvord, Jr, EC, Swanson AG. 1967 Hereditary and idiopathic types of diabetes insipidus. Brain. 90:707–714.[Free Full Text]
  27. Holmes MC, Catt KJ, Aguilera G. 1987 Involvement of vasopressin in the down-regulation of pituitary corticotropin-releasing factor receptors after adrenalectomy. Endocrinology. 121:2093–2098.[Abstract]
  28. Balment RJ, Brimble MJ, Forsling ML. 1982 Oxytocin release and renal action in normal and Brattleboro rats. Ann NY Acad Sci. 394:241–253.[Medline]
  29. Nussey SS, Ang VTY, Finer N, Jenkins JS. 1986 Responses of neurohypophysial peptides to hypertonic saline and insulin-induced hypoglycemia in man. Clin Endocrinol (Oxf). 24:97–105.[Medline]
  30. Williams TDM, Abel DC, King CMP, Jelley RY, Lightman SL. 1986 Vasopressin and oxytocin responses to acute and chronic osmotic stimuli in man. J Endocrinol. 108:163–168.[Abstract/Free Full Text]
  31. Spinedi E, Negro-Vilar A. 1983 Angiotensin II and ACTH release: site of action and potency relative to corticotropin releasing factor and vasopressin. Neuroendocrinology. 37:446–453.[Medline]
  32. Antaraki A, Rangou D, Chlouverakis C. 1994 The renin-aldosterone axis in patients with diabetes insipidus. Clin Endocrinol (Oxf). 40:505–510.[Medline]
  33. Ruskoaho H. 1992 Atrial natriuretic peptide: synthesis, release, and metabolism. Pharmacol Rev. 44:479–602.[Medline]
  34. Kamoi K, Ebe T, Kobayashi O, et al. 1990 Atrial natriuretic peptide in patients with the syndrome of inappropriate antidiuretic hormone secretion and with diabetes insipidus. J Clin Endocrinol Metab. 70:1385–1390.[Abstract]
  35. Antunes-Rodrigues J, Ramalho MJ, Reis LC, et al. 1991 Lesions of the hypothalamus and pituitary inhibit volume-expansion-induced release of atrial natriuretic peptide. Proc Natl Acad Sci USA. 88:2956–2960.[Abstract/Free Full Text]
  36. Haanwinckel MA, Elias LLK, Favaretto ALV, Gutkowska J, McCann SM, Antunes-Rodrigues J. 1995 Oxytocin mediates atrial natriuretic peptide release and natriuresis after volume expansion in the rat. Proc Natl Acad Sci USA. 92:7902–7906.[Abstract/Free Full Text]



This article has been cited by other articles:


Home page
 Exp PhysiolHome page
W. L. Reis, A. Giusti-Paiva, R. R. Ventura, L. O. Margatho, D. A. Gomes, L. L. K. Elias, and J. Antunes-Rodrigues
Neuroendocrinology/Endocrinology: Central nitric oxide blocks vasopressin, oxytocin and atrial natriuretic peptide release and antidiuretic and natriuretic responses induced by central angiotensin II in conscious rats
Exp Physiol, September 1, 2007; 92(5): 903 - 911.
[Abstract] [Full Text] [PDF]

Home page
 Exp PhysiolHome page
A. P. de Magalhaes-Nunes, D. Badaue-Passos Jr, R. R. Ventura, D. da Silva Guedes Jr, J. P. Araujo, P. C. Granadeiro, H. K. Milanez-Barbosa, R. H. da Costa-e-Sousa, M. A. de Medeiros, J. Antunes-Rodrigues, et al.
Neuroendocrinology/Endocrinology: Sertraline, a selective serotonin reuptake inhibitor, affects thirst, salt appetite and plasma levels of oxytocin and vasopressin in rats
Exp Physiol, September 1, 2007; 92(5): 913 - 922.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
L. O. Margatho, A. Giusti-Paiva, J. V. Menani, L. L. K. Elias, L. M. Vivas, and J. Antunes-Rodrigues
Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion
Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2007; 292(3): R1190 - R1197.
[Abstract] [Full Text] [PDF]

Home page
 Exp PhysiolHome page
F. V. Durlo, M. Castro, L. L. K. Elias, and J. Antunes-Rodrigues
Interaction of prolactin, ANPergic, oxytocinergic and adrenal systems in response to extracellular volume expansion in rats
Exp Physiol, September 1, 2004; 89(5): 541 - 548.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
J. ANTUNES-RODRIGUES, M. DE CASTRO, L. L. K. ELIAS, M. M. VALENCA, and S. M. McCANN
Neuroendocrine Control of Body Fluid Metabolism
Physiol Rev, January 1, 2004; 84(1): 169 - 208.
[Abstract] [Full Text] [PDF]

Home page
 J. Clin. Endocrinol. Metab.Home page
E. Itagaki, S. Ozawa, S. Yamaguchi, K. Ushikawa, T. Tashiro, H. Katahira, M. Takizawa, K. Yoshimoto, S. Murakawa, and H. Ishida
Increases in Plasma ACTH and Cortisol after Hypertonic Saline Infusion in Patients with Central Diabetes Insipidus
J. Clin. Endocrinol. Metab., December 1, 2001; 86(12): 5749 - 5754.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
A. Lacroix, N. N'Diaye, J. Tremblay, and P. Hamet
Ectopic and Abnormal Hormone Receptors in Adrenal Cushing's Syndrome
Endocr. Rev., February 1, 2001; 22(1): 75 - 110.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
P. A. Deuster, J. S. Petrides, A. Singh, G. P. Chrousos, and M. Poth
Endocrine Response to High-Intensity Exercise: Dose-Dependent Effects of Dexamethasone
J. Clin. Endocrinol. Metab., March 1, 2000; 85(3): 1066 - 1073.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
R. Pivonello, A. Faggiano, C. Di Somma, M. Klain, M. Filippella, M. Salvatore, G. Lombardi, and A. Colao
Effect of a Short-Term Treatment with Alendronate on Bone Density and Bone Markers in Patients with Central Diabetes Insipidus
J. Clin. Endocrinol. Metab., July 1, 1999; 84(7): 2349 - 2352.
[Abstract] [Full Text]

Home page
 J. Clin. Endocrinol. Metab.Home page
R. Pivonello, A. Colao, C. Di Somma, G. Facciolli, M. Klain, A. Faggiano, M. Salvatore, and G. Lombardi
Impairment of Bone Status in Patients with Central Diabetes Insipidus
J. Clin. Endocrinol. Metab., July 1, 1998; 83(7): 2275 - 2280.
[Abstract] [Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Submit a related Letter to the Editor
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Elias, L. L. K.
Right arrow Articles by Moreira, A. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Elias, L. L. K.
Right arrow Articles by Moreira, A. C.

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals