Skip to main content
SpringerLink
Log in

Selective Chronic Sodium or Chloride Depletion Specifically Modulates Subfornical Organ Atrial Natriuretic Peptide Receptor Number in Young Rats

  • Published:
Cellular and Molecular Neurobiology Aims and scope Submit manuscript

Abstract

1. We studied the effects of selective chronic sodium depletion of chloride depletion on atrial natriuretic peptide receptor number in the subfornical organ and paraventricular nucleus of young rats.

2. Sodium or chloride depletion decreased plasma levels of atrial natriuretic peptide, increased plasma renin activity, and induced extracellular fluid volume contraction. Chloride depletion induced more significant changes in extracellular fluid volume contraction than sodium depletion.

3. In the subfornical organ, atrial natriuretic peptide receptor number significantly decreased (30%) after sodium depletion, while chloride depletion induced a smaller, not statistically significant decrease. Conversely, atrial natriuretic peptide receptors located in the paraventricular nucleus of young rats were not significantly affected by sodium or chloride depletion.

4. Water deprivation reversed the decrease in atrial natriuretic peptide receptors produced by sodium depletion. Water-deprived sodium-depleted rats actually had higher numbers of atrial natriuretic peptide receptors in the subfornical organ than control rats. These changes were associated with severe extracellular fluid volume contraction and up regulation of brain vasopressin mRNA steady-state levels. Thus, the direction of change in the number of subfornical organ atrial natriuretic peptide receptors was dependent on the degree of extracellular fluid volume contraction.

5. Our results suggest that atrial natriuretic peptide receptors located in the subfornical organ, and not in the paraventricular nucleus, are selectively regulated by sodium depletion and extracellular fluid volume contraction.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

REFERENCES

  • American Institute of Nutrition (1977). Report of the American Institute of Nutrition. Ad Hoc. Committee on Standards for Nutritional Studies. J. Nutr. 107:1340–1348.

    Google Scholar 

  • Ballerman, B. J., and Brenner, B. M. (1985). Biological active atrial peptides. J. Clin. Invest. 76:2041–2048.

    Google Scholar 

  • Bradford, M. M. (1976). A rapid and sensitive method for quantification of microgram quantities of protein utilizing the principle of protein dye binding. Anal. Biochem. 72:248–254.

    Google Scholar 

  • Brown, J., and Zuo, Z. (1993). C-type natriuretic peptide and atrial natriuretic peptide receptors of rat brain. Am. J. Physiol. 264:R513–R523.

    Google Scholar 

  • Burnett, J. C., Granger, J. P., and Opgenorth, T. J. (1984). Effects of synthetic atrial natriuretic factor on renal function and renin release. Am. J. Physiol. 247:F863–F866.

    Google Scholar 

  • Castrén, E., and Saavedra, J. M. (1989). Lack of vasopressin increases hypothalamic atrial natriuretic peptide binding sites. Am. J. Physiol. 257:R168–R173.

    Google Scholar 

  • Davenport, A. P., and Hall, M. D. (1988). Comparison between brain paste and polymer 125I-standards for quantitative autoradiography. J. Neurosci. Methods 25:75–82.

    Google Scholar 

  • de Bold, A. J., Borenstein, H. B., Veress, A. T., and Sonnenberg, H. (1981). A rapid an potent natriuretic response to intravenous injection of atrial myocardial extract in rats. Life Sci. 28:89–94.

    Google Scholar 

  • Dillinham, M. A., and Anderson, R. J. (1986). Inhibition of vasopressin action by atrial natriuretic factor. Science 231:1572–1573.

    Google Scholar 

  • Gaillard, C. A., Mizelle, H. L., Montani, J. P., Brands, M. W., Hildebrandt, D. A., and Hall, J. E. (1990). Atrial natriuretic factor and blood pressure control; Role of sodium and aldosterone. Am. J. Physiol. 259:R973–R980.

    Google Scholar 

  • Goetz, K. L. (1988). Physiology and pathophysiology of atrial peptides. Am. J. Physiol. 254:E1–E15.

    Google Scholar 

  • Hisa, H., Tomura, Y., and Satoh, S. (1989). Atrial natriuretic factor suppress neural stimulation of renin release in dogs. Am. J. Physiol. 257:E332–E335.

    Google Scholar 

  • Iitake, K., Kimura, T., Ota, K., Shoji, M., Inoue, M., Ohta, M., Sato, K., Yamamoto, T., Yasujima, M., Abe, K., and Yoshinaga, K. (1989). Responses of vasopressin, atrial natriuretic peptide and blood pressure to central osmotic stimulation. Am. J. Physiol. 257:E611–E616.

    Google Scholar 

  • Koller, K. J., Lowe, D. G., Bennet, G. L., Minamino, N., Kangawa, K., Matsuo, H., and Goeddel, D. (1991). Selective activation of the B natriuretic peptide receptor by C-type natriuretic peptide (CNP). Science 252:120–123.

    Google Scholar 

  • Lattion, A. L., Aubert, J. F., Fluckiger, J. P., Nussberger, J., Waeber, B., and Brunner, H. R. (1988). Effect of sodium intake on gene expression and plasma levels of ANF in rats. Am. J. Physiol. 255:H245–H249.

    Google Scholar 

  • Menard, J., and Catt, K. J. (1972). Measurements of renin activity concentration and substrate in rat plasma by radioimmunoassay of angiotensin I. Endocrinology 90:424–430.

    Google Scholar 

  • Miller, A. J., Curella, P., and Zahniser, N. R. (1988). A new densitometric procedure to measure protein levels in tissue slices used in quantitative autoradiography. Brain Res. 447:60–66.

    Google Scholar 

  • Nakao, K., Ogawa, Y., Suga, S., and Imura, H. (1992). Molecular biology and biochemistry of the natriuretic peptide system. II. Natriuretic peptide receptors. J. Hypertens. 10:1111–1114.

    Google Scholar 

  • Nazarali, A. J., Gutkind, J. S., and Saavedra, J. M. (1989). Calibration of 125I-polymer standards with 125I brain paste standards for use in quantitative receptor autoradiography. J. Neurosci. Methods 30:247–253.

    Google Scholar 

  • Palkovits, M., Essay, R. L., and Antoni, F. A. (1987). Atrial natriuretic peptide in the median eminence is of paraventricular nucleus origin. Neuroendocrinology 46:542–544.

    Google Scholar 

  • Paul, R. V., Kirk, K. A., and Navar, L. G. (1987). Renal autoregulation and pressure natriuresis during ANF-induced diuresis. Am J. Physiol. 253:F424–F431.

    Google Scholar 

  • Paxionos, G., and Watson, C. (1986). The Rat Brain in Stereotaxic Coordinates, Academic Press, New York.

    Google Scholar 

  • Rauch, A. L., Callahan, M. F., Buckalew, V. M., and Morris, M. (1990). Regulation of plasma atrial natriuretic peptoide by the central nerovus system. Am. J. Physiol. 258:R531–R535.

    Google Scholar 

  • Ray, P. E., Castrén, E., Ruley, E. J., and Saavedra, J. M. (1990a). Different effects of sodium or chloride depletion on angiotensin II receptors in rats. Am. J. Physiol. 258:R1008–R1015.

    Google Scholar 

  • Ray, P. E., Ruley, E. J., and Saavedra, J. M. (1990b). Down regulation of angiotensin II receptors in subfornical organ or young male rats by chronic sodium depletion. Brain Res. 510:303–308.

    Google Scholar 

  • Ray, P. E., Caster, E., Ruley, E. J., and Saavedra, J. M. (1991). Different effects of chronic sodium, chloride and potassium depletion on brain vasopressin mRNA and plasma vasopressin in young rats. Cell. Mol. Neurobiol. 11:277–287.

    Google Scholar 

  • Rohmeiss, P., Demmert, G., and Unger, T. (1991). Central effects of atrial natriuretic factor on renal salt excretion. Am. J. Physiol. 26:F354–F359.

    Google Scholar 

  • Robertson, G. L., Mahr, E. A., Athar, S., and Sinha, T. (1973). Development and clinical application of a new method for the radioimmunoassay of arginine vasopressin in human plasma. J. Clin. Invest. 52:2340–2353.

    Google Scholar 

  • Saavedra, J. M., Correa, F. M. A., Plunkett, L. M., Israel, A., Kurihara, M., and Shigematsu, K. (1986a). Binding of Angiotensin and atrial natriuretic peptide in brain of hypertensive rats. Nature 320:758–760.

    Google Scholar 

  • Saavedra, J. M., Israel, A., Correa, F. M. A., and Kurihara, M. (1986b). Increased atrial natriuretic peptide (6–33) binding sites in the subfornical organ of water deprived and Brattleboro rats. Proc. Soc. Exp. Biol. Med. 182:559–563.

    Google Scholar 

  • Samson, W. K. (1985). Dehydration-induced alterations in rat brain vasopressin and atrial natriuretic factor immunoreactivity. Endocrinology 1217:1279–1281.

    Google Scholar 

  • Saper, C. B., Standaert, D. G., Currie, M. G., Schwartz, D., Geller, D. M., and Needleman, P. (1985). Atriopeptin-immunoreactive neurons in the brain: Presence in cardiovascular regulatory areas. Science 227:1047–1049.

    Google Scholar 

  • Scheuer, D. A., Thrasher, T. N., Keil, L. C., and Ramsay, D. J. (1989). Mechanism of inhibition of renin response to hypotension by atrial natriuretic factor. Am. J. Physiol. 257:R194–R203.

    Google Scholar 

  • Steardo, L., and Nathanson, J. A. (1987). Brain barrier tissues: end organs for atriopeptins. Science 235:470–473.

    Google Scholar 

  • Zorad, S., and Saavedra, J. M. (1993). Quantitative autoradiography analysis of brain atrial natriuretic peptides receptors. In Parvez, S. H., Naoi, M., Nagatsu, T., and Parvez, S. (eds.), Methods in Neurotransmitter and Neuropeptide Research, Elsevier Science, Amsterdam, pp. 431–441.

    Google Scholar 

  • Zorad, S. K., Tsutsumi, K., and Saavedra, J. M. (1992). Selective localization of C atrial natriuretic peptide receptors in the rat brain. Brain Res. 570:149–153.

    Google Scholar 

  • Zorad, S., Tsutsumi, K., Bhatia, A. J., and Saavedra, J. M. (1993). Localization and characterization of atrial natriuretic peptide receptors in prenatal and postnatal rat brain. Eur. J. Pharmacol. 241:195–200.

    Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Department of Nephrology and Center IV, Children's Research Institute, Children's National Medical Center and The George Washington University, Washington, DC

    Patricio E. Ray

  2. Section on Pharmacology, Laboratory of Clinical Science, National Institute of Mental Health, Bethesda, Maryland

    Juan M. Saavedra

Authors
  1. Patricio E. Ray
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Juan M. Saavedra
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Ray, P.E., Saavedra, J.M. Selective Chronic Sodium or Chloride Depletion Specifically Modulates Subfornical Organ Atrial Natriuretic Peptide Receptor Number in Young Rats. Cell Mol Neurobiol 17, 455–470 (1997). https://doi.org/10.1023/A:1026302703894

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1023/A:1026302703894

Search

Navigation