This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow P3Rs: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when P3Rs are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow E-mail 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 Add to My File Cabinet
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via CrossRef
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Legris, G. J.
Right arrow Articles by Doershuk, C. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Legris, G. J.
Right arrow Articles by Doershuk, C. F.
Related Collections
Right arrow Respiratory Tract

PEDIATRICS Vol. 101 No. 1 January 1998, pp. 48-56

Sodium Space and Intravascular Volume: Dietary Sodium Effects in Cystic Fibrosis and Healthy Adolescent Subjects

Received Apr 9, 1996; accepted May 30, 1997.

Gregory J. Legris, Dorr Dearbornparallel , Robert C. Stern*, parallel , Cynthia L. Geiss, Ulrich HopferDagger , Janice G. Douglasparallel , and Carl F. Doershuk*, parallel

From the Departments of * Pediatrics, Dagger  Physiology and Biophysics, and § Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio; parallel  Leroy W. Matthews Cystic Fibrosis Center, Rainbow Babies and Children's Hospital, University Hospitals of Cleveland, Cleveland, Ohio; and  St Joseph's Hospital and Medical Center, Phoenix, Arizona.

Objective.  To assess the physiologic response to salt depletion in subjects with cystic fibrosis (CF) and control male adolescents for sodium balance, sodium space, and stimulation of the renin-angiotensin-aldosterone axis.

Design.  Seven subjects with CF and six controls received a salt-replete (150 or 290 mmol NaCl per day) diet and then a salt-deplete (10 mmol NaCl per day) diet while in a clinical research center.

Results.  Space maintenance: CF subjects responded to salt depletion with a greater weight loss than did controls (1.9 vs 0.8 kg) and a decrease in 24Na+ space, whereas controls maintained 24Na+ space. Paired (Na-deplete/Na-replete) blood volumes decreased in subjects with CF, but not in controls. Renin-angiotensin-aldosterone axis stimulation: During salt repletion, subjects with CF had significantly higher aldosterone values than did controls in the afternoon, but not at 7:00 AM. During salt depletion, plasma renin activity and aldosterone increased significantly more in subjects with CF than in controls (renin, 35 vs 13 ng/mL/hour [9.7 vs 3.6 ng·L-1 s-1]; aldosterone: 181 vs 101 ng/dL [5021 vs 2802 pmol/L]). Furthermore, the angiotensin antagonist saralasin increased renin much more in subjects with CF (154 vs 36 ng/mL per hour [43 vs 10 ng·L-1 s-1]). Vasomotor functions: Mean arterial pressure was decreased in subjects with CF on both diets and decreased significantly more with low salt only in subjects with CF. During salt depletion, subjects with CF showed enhanced orthostatic tolerance (less heart rate increase with standing) compared with controls, thus obscuring their volume loss. The blood pressure response to an acute infusion of saralasin suggested that in salt-replete subjects with CF, but not in controls, angiotensin receptors were functional in maintaining vascular tone. During salt depletion, angiotensin was more important for maintenance of blood pressure in subjects with CF than in controls, because the saralasin-induced drop in blood pressure was 20%, ie, close to shock levels, in subjects with CF, and only 6% in controls.

Conclusion.  The data suggest that patients with CF are so successful in compensating for volume depletion by vigorous activation of the renin-angiotensin system that salt depletion/dehydration cannot be recognized easily by routine clinical measurements, eg, capillary refill, serum sodium levels, or tachycardia.

Key words: dietary sodium chloride, cystic fibrosis.




This article has been cited by other articles:


Home page
 HypertensionHome page
M. Super, A. Irtiza-Ali, S. A. Roberts, M. Schwarz, M. Young, A. Smith, T. Roberts, J. Hinks, and A. Heagerty
Blood Pressure and the Cystic Fibrosis Gene: Evidence for Lower Pressure Rises With Age in Female Carriers
Hypertension, December 1, 2004; 44(6): 878 - 883.
[Abstract] [Full Text] [PDF]

Home page
 CLIN PEDIATRHome page
J. B. Lasekan, K. M. Ostrom, J. R. Jacobs, M. M. Blatter, L. I. Ndife, W. M. Gooch III, and S. Cho
Growth of Newborn, Term Infants Fed Soy Formulas For 1 Year
Clinical Pediatrics, October 1, 1999; 38(10): 563 - 571.
[Abstract] [PDF]