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   <subfield code="u">Committee on Clinical Pharmacology, Department of Pharmacological and Physiological Sciences, The University of Chicago, 947 East 58th Street, 60637, Chicago, IL, USA</subfield>
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   <subfield code="a">Presynaptic effects of dopexamine hydrochloride in the canine kidney</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Alan Bass]</subfield>
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   <subfield code="a">Summary: The effects of dopexamine on the vasoconstrictor response to renal nerve stimulation and noradrenaline were determined in anesthetized dogs. Renal vasoconstriction was repeated during the sequential administration of iso-osmotic saline, dopexamine, dopexamine plus the DA1-dopamine receptor antagonist, SCH 23390, and dopexamine plus SCH 23390 and the DA2-dopamine receptor antagonist, domperidone. Renal nerve stimulation-induced vasoconstriction did not change with dopexamine or dopexamine plus SCH 23390, but increased with the addition of domperidone. Dopexamine also potentiated noradrenaline-induced vasoconstriction. Antagonists alone had no affect on the vasoconstrictor response to either stimulus. The findings suggest that the absence of an effect of dopexamine on neuronally-induced renal vasoconstriction was a consequence of a balance between its actions at presynaptic DA2-dopamine receptors (attenuated vasoconstriction) and its ability to inhibit the uptake, transporter (enhanced vasoconstriction).</subfield>
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   <subfield code="a">Dopamine receptors</subfield>
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   <subfield code="a">Renal nerves</subfield>
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