Why the study?
Does dopamine D3 receptor activation affect renal hemodynamics in anesthetized rats?
Does dopamine D3 receptor activation affect renal hemodynamics in anesthetized rats?
Pharmacological activation of dopamine D3 receptors induces preferential postglomerular vasoconstriction, altering renal hemodynamics in anesthetized rats.
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D3 activation may alter rat renal hemodynamics; hypothesis-generating for human relevance and requires clinical translation studies.
In the present study we investigated the renal hemodynamic effects of dopamine D(3) receptor activation by R(+)-7-hydroxy-dipropylaminotetraline (7-OH-DPAT) in thiopental-anesthetized Sprague-Dawley rats. In clearance experiments infusion of 7-OH-DPAT (0.01-1.0 microg. kg(-1). min(-1)) 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 microg. kg(-1). min(-1)) increased GFR by 16 +/- 2%, associated with an unexpected fall in renal blood flow by 20 +/- 3% and a significant elevation of renal vascular resistance by 18 +/- 3%. The renal hemodynamic changes were not influenced by pretreatment with the D(2)-receptor antagonist S(-)-sulpiride but were completely abolished during D(3) receptor inhibition by 5,6-dimethoxy-2-(di-n-propylamino)indane (U-99194A). In micropuncture experiments 7-OH-DPAT (1.0 microg. kg(-1). min(-1)) 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 D(3) receptors affects renal hemodynamics in anesthetized rats by preferential postglomerular vasoconstriction.
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Luippold et al. (2000) studied this question.
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