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Neural not tubular dopamine increases glomerular filtration rate in perfused rat kidneys.

We examined the effect of endogenous neural and tubular dopamine production on renal function in isolated perfused kidneys. Nerves and proximal tubules in perfused kidneys produce dopamine from endogenous substrates. Surgical denervation 5-14 days before perfusion removed neural dopamine production and decreased dopamine excretion 32% (P less than 0.05), inulin clearance 7% (P less than 0.05), and sodium excretion 57% (P less than 0.01). Carbidopa, which abolished neural and tubular dopamine production, produced similar functional effects. Haloperidol, Sch 23390, and (+)butaclamol, but not (-)butaclamol, added during perfusion increased renovascular resistance 4-5% (P less than 0.001) and decreased inulin clearance 20% (P less than 0.001). Sch 23390 reduced fractional sodium excretion (P less than 0.01), but haloperidol and butaclamol did not. Chronic denervation or carbidopa blocked the reduction of inulin clearance by haloperidol, but alpha- and beta-adrenergic antagonists did not. Fractional sodium excretion increased after adding haloperidol to denervated or adrenergic blocked kidneys. Denervation blocked the effect of Sch 23390 on inulin clearance but not on sodium excretion. Haloperidol inhibited dopamine excretion. Thus dopamine released from acutely severed nerves in perfused kidneys increases glomerular filtration rate (GFR). Dopamine produced by tubules of chronically denervated kidneys did not influence GFR but stimulated sodium excretion by an Sch 23390-sensitive mechanism.