The kidneys dictate sodium excretion and reabsorption with precision, typically reabsorbing over 99 per cent of some 25 000 mmol of sodium filtered daily through the glomeruli. An increment in salt intake induces water retention and a subsequent transient gain in body weight until a compensatory increase in urinary sodium excretion ensues. Opposite effects are observed when sodium intake is reduced. Control of sodium excretion is mainly dependent on glomerular filtration rate and sodium reabsorption, modulated by various hormones. Extracellular fluid volume, not extracellular fluid sodium, is the critical factor determining sodium balance.
A decrease in absolute or effective blood volume and a subsequent decline in arterial blood pressure precipitate a decrease in renal perfusion pressure (renal plasma flow) and glomerular filtration rate. The decline in glomerular filtration rate is proportionally less than the drop in renal plasma flow, yielding an increase in the filtration fraction (ratio of glomerular filtration rate to renal plasma flow) and in the protein concentration in the efferent arterioles and peritubular capillaries. Sympathetic activity consequent upon a drop in blood pressure induces renal vasoconstriction. The decline in glomerular filtration rate diminishes sodium filtration and excretion, while catecholamines augment proximal tubule sodium reabsorption. Stimulation of angiotensin II during episodes of volume depletion vasoconstricts mostly the glomerular efferent arterioles, preserving glomerular filtration rate, but reduces peritubular capillary hydrostatic and interstitial pressure. This pressure reduction, combined with the increase in peritubular capillary protein concentration, facilitates sodium and water reabsorption in the proximal tubules during hypovolemia. Extracellular fluid volume expansion results in opposite compensatory effects (Va.Od.e.L1991).
Endocrine effects on sodium regulation are illustrated in Table...,1...
Table 1 Endocrine effects on sodium regulation
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