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Am J Physiol Regul Integr Comp Physiol (February 14, 2002). doi:10.1152/ajpregu.00732.2001
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Articles in PresS, published online ahead of print February 14, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00732.2001
Submitted on December 7, 2001
Accepted on February 2, 2002

NATRIURESIS INDUCED BY MILD HYPERNATREMIA IN HUMANS

Lars Juel Andersen1, Jens Lundbaek Andersen2, Bettina Pump3, and Peter Bie4*

1 Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark; Department of Clinical Physiology, Herlev Hospital, Copenhagen, Denmark
2 Department of Medical Physiology, University of Copenhagen, Copenhagen, Denmark
3 Department of Aviation Medicine, Rigshospitalet, Copenhagen, Denmark
4 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark

* To whom correspondence should be addressed. E-mail: pbie{at}health.sdu.dk.

The hypothesis that increases in the plasma sodium induce natriuresis independent of changes in body fluid volume was tested in 6 slightly dehydrated seated subjects on controlled sodium intake (150 mmol/day). NaCl (3.85 mmol/kg) was infused intravenously over 90 min as isotonic (ISO) or as hypertonic saline (HYPER, 855 mmol/l). Following HYPER, plasma sodium increased by 3 % (142.0±0.6 to 146.2±0.5 mmol/l). During ISO a small decrease occurred (142.3±0.6 to 140.3±0.7 mmol/l). ISO increased estimates of plasma volume significantly more than HYPER. However, renal sodium excretion increased significantly more with HYPER (291±25 versus 199±24 µmol/min). This excess was not mediated by arterial pressure, which actually decreased slightly. Creatinine clearance did not change measurably. Plasma renin activity, angiotensin II and aldosterone decreased very similarly in ISO and HYPER. Plasma atrial natriuretic peptide remained unchanged, whereas plasma vasopressin increased with HYPER (1.4±0.4 to 3.1±0.5 pg/ml) and decreased (1.3±0.4 to 0.6±0.1 pg/ml) following ISO. In conclusion, the natriuretic response to HYPER was 50% larger than to ISO indicating that renal sodium excretion may be determined partly by plasma sodium concentration. The mechanism is uncertain but appears independent of changes in blood pressure, glomerular filtration rate, the renin system, and atrial natriuretic peptide.




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