Issue title: Proceedings of the Seventh International Congress of Biorheology. Part I. Palais des Congrès, Nancy, France, 18–23 June 1989. Dedicated to Richard Skalak
Guest editors: Alfred L. Copley and Jean-François Stoltz
Affiliations: Depts. of AMES-Bioengineering and Medicine, Univ. Calif. San Diego, CA 92093; and Dept. of Physiology and Cellular Biophysics and Dept. of Medicine, Columbia Univ. College of Physicians and Surgeons, New York, NY 10032, U.S.A.
Note: [] Accepted by:
Abstract: The effects of alterations in blood and plasma viscosities on plasma renin activity (PRA) were studied in dogs anesthetized with pentobarbital. Blood viscosity was altered by changing the hematocrit (Hct) level by isovolemic exchange using packed red blood cells or plasma. Plasma viscosity was elevated by isovolemic exchange using Hct-matched blood with high molecular weight dextran (Dx, mean m.w. ∼450,000) dissolved in plasma. Following control measurements of plasma and blood viscosities, plasma [Dx], PRA, Hct and hemodynamic functions, the dog was subjected to isovolemic exchange transfusions to either alter the Hct or administer the Dx. Various measurements were repeated 40–60 min after each exchange. Arterial pressure and renal blood flow remained relatively constant after exchanges; increases in plasma and blood viscosities were accompanied by a decrease in renal vascular hindrance (vasodilation) to keep the renal flow resistance at control level. PRA rose with increases in plasma [Dx] and viscosity, and the rise in PRA was best correlated with the decrease in renal hindrance. The changes in PRA and renal hindrance have the same regression line whether blood viscosity was altered by Hct variation or Dx administration. The results indicate that increases in viscosity cause a compensatory vasodilation of renal vessels to cause renin secretion.
