AFLUID April 47/4

Luippold, Gerd, Swetlana Schneider, Volker Vallon, Hartmut Osswald, and Bernd Mühlbauer. Postglomerular vasoconstriction induced by dopamine D3 receptor activation in anesthetized rats. Am J Physiol Renal Physiol 278: F570–F575, 2000.—In the present study we investigated the renal hemodynamic effects of dopamine D3 receptor activation by R(1)-7-hydroxy-dipropylaminotetraline (7-OH-DPAT) in thiopental-anesthetized Sprague-Dawley rats. In clearance experiments infusion of 7-OH-DPAT (0.01–1.0 μg·kg21 ·min21) dose-dependently elevated glomerular filtration rate (GFR) without affecting mean arterial blood pressure (MAP). In renal blood flow experiments 7-OH-DPAT infusion (1.0 μg·kg21 ·min21) increased GFR by 16 6 2%, associated with an unexpected fall in renal blood flow by 20 6 3% and a significant elevation of renal vascular resistance by 18 6 3%. The renal hemodynamic changes were not influenced by pretreatment with the D2-receptor antagonist S(2)sulpiride but were completely abolished during D3 receptor inhibition by 5,6-dimethoxy-2-(di-n-propylamino)indane (U99194A). In micropuncture experiments 7-OH-DPAT (1.0 μg·kg21 ·min21) significantly elevated stop-flow pressure measured in the early proximal tubules and reduced hydrostatic pressure at the first branching point of the efferent arteriole without altering MAP. We conclude from these data that pharmacological activation of dopamine D3 receptors affects renal hemodynamics in anesthetized rats by preferential postglomerular vasoconstriction.