Pharmacological characterization of renal vascular dopamine receptors.
We present an in vitro method for studying the renal effects of dopamine in the isolated rat kidney. The organ is perfused in an open circuit and can be maintained satisfactorily for up to 180 min. The responses to dopamine were studied in the presence of phenoxybenzamine (10(-5) M) and sotalol (10(-5) M) while stable renal vasoconstriction was maintained by perfusion with prostaglandine F2 alpha. Dopamine induced dose-dependent renal vasodilation with an ED50 of 2.53 X 10(-6) moles/liter, which was not modified by reserpine pretreatment. (+) Butaclamol but not (-) butaclamol shifted the dopamine dose-response curve to the right in a parallel fashion, indicating competitive antagonism. Haloperidol and sulpiride at concentrations without intrinsic effect on vascular resistance also acted as competitive inhibitors for dopamine. Calculation of empirical pA2 values yielded the following relative potencies for these antagonists: (+) butaclamol greater than haloperidol greater than sulpiride. The renal vascular dopamine receptors are tentatively classified as being of the D1 type.
D000818:Animals; D002069:Butaclamol / Q000494:pharmacology; D004298:Dopamine / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D006220:Haloperidol / Q000494:pharmacology; D007668:Kidney / Q000098:blood supply*; D008297:Male; D011460:Prostaglandins F / Q000494:pharmacology; D051381:Rats; D011954:Receptors, Dopamine / Q000187:drug effects*; D012039:Regional Blood Flow / Q000187:drug effects; D013469:Sulpiride / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects
D011460:Prostaglandins F; D011954:Receptors, Dopamine; D013469:Sulpiride; D002069:Butaclamol; D006220:Haloperidol; D004298:Dopamine