Key result
Dopamine induces dose-dependent renal vasodilation via D1 receptors competitively blocked by butaclamol, haloperidol, and sulpiride.
Why the study?
The renal vascular dopamine receptors have not been fully characterized pharmacologically in an isolated rat kidney model.
Does dopamine induce renal vasodilation in isolated rat kidneys, and what type of receptors mediate this effect?
Population
Isolated rat kidney model
Comparison
Dopamine with phenoxybenzamine and sotalol versus dopamine with antagonists (+) butaclamol, (-) butaclamol, haloperidol, sulpiride
Design
In vitro pharmacological study
Follow-up
Up to 180 min
Authors
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Does not support changes in clinical dopamine use; extends D1 mediation evidence to isolated rat kidneys.
Does dopamine induce renal vasodilation in isolated rat kidneys, and what type of receptors mediate this effect?
Dopamine induces dose-dependent renal vasodilation in isolated rat kidneys mediated by D1-type receptors.
Schmidt et al. (1980) studied this question. Dopamine vs. Antagonists ((+) butaclamol, haloperidol, sulpiride) was evaluated on Renal vasodilation. Dopamine induced dose-dependent renal vasodilation that was competitively antagonized by (+) butaclamol, haloperidol, and sulpiride, indicating D1 type receptors.
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