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

Abstract

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 (ΔBP; +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 ΔBP (+12 mmHg) without changing HR. IsoLoad during vasopressin clamping (constant vasopressin infusion) caused comparable natriuresis at augmented ΔBP (+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 ΔBP (+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.