Contrasting effects of dopexamine hydrochloride on electrolyte excretion in canine kidney.

Renal responses to dopexamine were determined in anesthetized dogs in the absence and presence of dopamine receptor (DA1) and beta-2-adrenoceptor (beta-2) blockade. Dopexamine increased the rate of urine flow (V) and sodium excretion (UNaV) without affecting the fractional excretion of sodium (FENa) or the urinary (UKV) and fractional (FEK) excretions of potassium. Glomerular filtration rate (GFR) was increased and renal vascular resistance (RVR) reduced by the drug. With infusion of the DA1 antagonist, SCH 23390, dopexamine decreased V, UNaV, FENa, UKV and FEK. The agonist-induced increase in GFR and decrease in RVR were blocked. In the presence of the beta-2 antagonist, ICI 118551, dopexamine increased V, UNaV, FENa UKV and FEK; RVR was reduced, whereas GFR remained unchanged. SCH 23390, combined with ICI 118551, blocked the renal responses to dopexamine. During sample collection, dopexamine did not significantly affect mean arterial pressure in any group. In conclusion, the actions of dopexamine at DA1 and beta-2 receptors produce opposing changes in electrolyte excretion. Its combined actions at these receptors produces an increase in UNaV, attributed to an increase in glomerular filtration.