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. KEY WORDS plasma colloid hyperviscosity sodium excretion blood rheology dextran systemic hemodynamics• One of the well-documented responses to renal artery constriction is an increase in renin secretion by the kidney (1, 2). This observation implies that the mechanisms controlling renin secretion are responsive to changes in renal vascular resistance, although how the response is mediated is still a source of controversy (3, 4). Blood vessel diameter is of prime importance in determining flow resistance, but another determinant, blood viscosity, also contributes significantly to resistance, as predicted by the Poiseuille equation. The question arises, therefore, whether changes in blood viscosity might also influence renin secretion.Whole blood viscosity is determined chiefly by the hematocrit and the colloidal components of plasma (5). In a recent preliminary report, McDonald and Smith (6) 112 in renin secretion. The present study was designed to examine the mechanisms mediating this response and to compare it with the effects of colloid-induced hyperviscosity. In one group of dogs the hematocrit was increased, and the magnitude of the resulting rise in blood viscosity was measured by cone-plate viscometry. In another group of dogs similar changes in viscosity were produced by infusing high-molecular weight dextran, while blood volume and hematocrit were kept constant. This procedure allowed a comparison to be made between the effects of hematocrit-induced and colloid-induced changes in blood rheology on renin secretion, renal hempdynamics, and sodium excretion. MethodsMo...