Effect of hematocrit and colloid-induced changes in blood viscosity on renal hemodynamics and renin release in the dog.

This study compared the effects on the kidney of two major determinants of blood viscosity, the hematocrit and the plasma colloid content. In anesthetized dogs, blood viscosity was raised 30% by increasing hematocrit or infusing isoncotic Dextran 500 while blood volume was kept constant. Neither form of hyperviscosity altered blood pressure, but both forms caused a decrease of about 35% in cardiac output and a comparable rise in total peripheral resistance. Renal blood flow decreased minimally (<10%) in the group of dogs with increased hematocrit but fell more than 30% in the group given Dextran 500. Reciprocal changes occurred in renal vascular resistance. The increase in hematocrit was accompanied by an increase in renin secretion from 146 units/min to 416 units/min (P< 0.001), but Dextran 500 caused a decrease from 167 units/min to 107 units/min (P< 0.025). Sodium and potassium excretion both decreased similarly in the two groups. The data suggest that increased hematocrits are accompanied by renal vasodilatation so that renal vascular resistance rises less than blood viscosity. Dextran hyperviscosity, however, causes no compensatory vasodilatation. This difference in renal vascular response might explain the difference in renin secretion; afferent arteriolar dilatation might stimulate renin release during a rise in hematocrit, and the absence of vasodilatation in colloid hyperviscosity might explain its failure to stimulate renin.