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Am J Physiol Regul Integr Comp Physiol 278: R1-R10, 2000;
0363-6119/00 $5.00
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Vol. 278, Issue 1, R1-R10, January 2000

Determinants of the natriuresis after acute, slow sodium loading in conscious dogs

Peter Bie1 and Niels C. F. Sandgaard2

2 Department of Medical Physiology, University of Copenhagen, DK-2200 Copenhagen; and 1 Department of Physiology and Pharmacology, University of Southern Denmark, Odense, DK-5000 Odense, Denmark

The relative importance of systemic volume, concentration, and pressure signals in sodium homeostasis was investigated by intravenous infusion of isotonic (IsoLoad) or hypertonic (HyperLoad) saline at a rate (1 µmol Na+ · kg-1 · s-1), similar to the rate of postprandial sodium absorption. IsoLoad decreased plasma vasopressin (-35%) and plasma ANG II (-77%) and increased renal sodium excretion (95-fold), arterial blood pressure (Delta BP; +6 mmHg), and heart rate (HR; +36%). HyperLoad caused similar changes in plasma ANG II and sodium excretion, but augmented vasopressin (12-fold) and doubled Delta BP (+12 mmHg) without changing HR. IsoLoad during vasopressin clamping (constant vasopressin infusion) caused comparable natriuresis at augmented Delta BP (+14 mmHg), but constant HR. Thus vasopressin abolished the Bainbridge reflex. IsoLoad during normotensive angiotensin clamping (enalaprilate plus constant angiotensin infusion) caused marginal natriuresis (9% of unclamped response) despite augmented Delta BP (+14 mmHg). Cessation of angiotensin infusion during IsoLoad immediately decreased BP (-13 mmHg) and increased glomerular filtration rate by 20% and sodium excretion by 45-fold. The results suggest that fading of ANG II is the cause of acute "volume-expansion" natriuresis, that physiological ANG II deviations override the effects of modest systemic blood pressure changes, and that endocrine rather than hemodynamic mechanisms are the pivot of normal sodium homeostasis.

volume expansion; arterial blood pressure; angiotensin II; vasopressin; atrial natriuretic peptide


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