Effects of salt intake and renal denervation on catecholamine catabolism and excretion

My study was designed to measure the effect of salt intake on secretion and catabolism of catecholamines by the kidney and renal nerve contributions to urinary catecholamine excretion. Rats with one chronically denervated (DEN) and one innervated (INN) kidney were fed either high salt (HS) or low salt (LS) diets for 5 to 14 days. Under Inactin anesthesia rats were expanded with isotonic saline while LS rats received 10% mannitol to produce the same urine flow rates. Epinephrine excretion was ten times greater from LS than from HS rats; however, epinephrine/inulin excretion was the same from INN and DEN kidneys. Norepinephrine/inulin excretion was 30% less from DEN than from INN kidneys in both HS and LS rats (P less than 0.01). Dopamine/inulin excretion was 20% less from the DEN kidney than from the INN kidney of HS rats (P less than 0.05), but the 5% lower dopamine/inulin excretion from DEN than from INN of LS rats was not significant. Norepinephrine and dopamine tubular secretions from the rats, estimated by microinjecting radioactive tracers beneath the renal capsule, were 21 and 65%, respectively. After the microinjection, 68% of radioactive norepinephrine and 65% of radioactive dopamine were secreted unchanged. Catecholamine secretion rates and catabolism were not altered by denervation or different salt intakes. Estimated neural NE release was 1 ng/min in INN kidneys of both HS and LS rats; dopamine release 0.6 ng/min in kidneys of HS rats. Thus, when anesthesized, renal nerves contribute 30% to urinary NE and up to 21% to urinary dopamine excretion. Salt intake did not influence NE release from renal nerves or catecholamine secretion and catabolism by the kidney, but salt depletion decreased the renal nerve contribution to urinary dopamine excretion.