Effect of Hematocrit and Colloid-Induced Changes in Blood Viscosity on Renal Hemodynamics and Renin Release in the Dog

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Abstract
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 (P 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.