Sodium Excretion during Acute Saline Loading in Dogs with Vena Caval Constriction*

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Abstract
The response to acute saline infusions was studied in 4 groups of dogs, all treated with large doses of mineralocorticoids: controls; TVC dogs, in which the inferior vena cava had been constricted in the thorax 2 to 8 days before study; AVC dogs, in which the vena cava had been constricted just above the renal veins 2 to 8 days before study; acute TVC dogs, in which the inferior vena cava had been constricted in the thorax 1 1/2 hours before study. In control dogs sodium excretion increased 860 uEq/min and glomerular filtration rate (GFR) increased 5 ml/min after 2 L of saline. In TVC dogs, sodium excretion increased only 48 uEq/min, in spite of an increase of 16 ml/min in GFR. In AVC dogs, sodium excretion increased 343 uEq/min; GFR was variable, but, on the average, unchanged. In 7 paired experiments, the same dog was studied as a control and as a TVC dog. In 5 dogs, GFR both before and after saline loading as a TVC dog was higher than in the control study, yet sodium excretion in the TVC studies was markedly reduced. There was little or no tendency for sodium excretion to increase in spite of increased GFR, even after progressive infusion of up to 4 L of saline in chronic TVC dogs. In acute TVC dogs, sodium excretion was 253 uEq/min above pre-saline values after 2 L of saline and increased progressively to 469 uEq/min above pre-saline levels after 4 L, in spite of decreased GFR. It is concluded that the striking sodium retention in chronic TVC dogs is not due to decreased basal or post-saline GFR. The decrease in tubular reabsorption of sodium that occurs in normal dogs after saline loading is not manifested in TVC dogs, either because it does not become operative or because it is masked by a potent opposing mechanism. The difference in response of the TVC and AVC dogs suggests hepatic regulation of sodium excretion.

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