Intrarenal hypertonic saline infusions in dogs with thoracic caval constriction

Abstract

Intrarenal artery infusions of hypertonic saline can activate tubuloglomerular feedback (TGF), decreasing renal blood flow (RBF) and glomerular filtration rate (GFR). The response to infusion of hypertonic saline is enhanced by salt depletion and attenuated by salt loading, but has not previously been investigated in pathophysiological states where expanded extracellular fluid volume due to salt retention is associated with avid, renal sodium reabsorption. The renal response following intrarenal infusions of hypertonic saline was investigated in five control dogs and eleven dogs with partial constriction of the thoracic portion of their inferior vena cava, which resulted in salt retention and the formation of ascites. Intrarenal infusion of hypertonic saline induced significant reductions in RBF and GFR in both control and caval constricted dogs. The extent of these reductions were positively correlated with baseline renal function. An intravenous infusion of 50 ml/kg of 0.9% sodium chloride, which abolished the vasoconstrictor response in normal dogs, failed to abolish the decrease in RBF and GFR in response to intrarenal hypertonic saline infusion in dogs with ascites which had an initial vasoconstrictor response. We conclude that the potential for TGF is preserved in early stages of caval constriction syndrome in dogs, but that this potential activity decreases when basal renal function decreases.