Urinary Excretion of Catechol Amines in the Rat After Their Liberation by Reserpine or Dexamphetamine

Abstract

Daily urinary excretion of catechol amines in normal rats and in rats from which the adrenal medullae had been removed has been determined by a photofluorimetric method. In both groups, reserpine (2 mg/kg, intraperitoneally) produces: (1) A decrease in the urinary excretion of noradrenaline which persists for more than 3 weeks; this action is not influenced by monoamine oxidase inhibitors and mecamylamine. (2) An increase, within 20 to 68 hr, in the urinary excretion of adrenaline, even though the urine of rats without adrenal medullae does not usually contain adrenaline. These effects are prevented by monoamine oxidase inhibitors and, in the normal animals, are reduced by mecamylamine. In both groups, dexamphetamine (6 mg/kg, intraperitoneally) produces an increase in the excretion of adrenaline and noradrenaline, the adrenaline appearing in the urine of the rats without adrenal medullae within 20 to 44 hr. Mecamylamine prevents the effect of dexamphetamine on the excretion of noradrenaline. Dexamphetamine, administered within a week of reserpine treatment, produces its usual effects on the urinary excretion of catechol amines in normal rats, but has no effect in rats without adrenal medullae. The results are discussed with regard to both the mechanism by which reserpine and dexamphetamine influence the peripheral stores of adrenaline and noradrenaline, and the significance of the adrenal and extra-adrenal chromaffin system.

Effects of guanethidine on the blood pressure response to splanchnic nerve stimulation in the rat: role of the adrenal medulla

“…Various explanations may be proposed. The possibility exists that damage to the splanchnic nerve occurred during the intervention on the adrenals; this, however, seems to be excluded by previous observations that adrenal demedullation is followed by an increase in the urinary output of noradrenaline; moreover, the same rise in the urinary excretion of this mediator is observed in intact as well as in adrenal-demedullated rats after an acute pharmacological stress (Biscardi, Carpi & Orsingher, 1964). Adrenocortical insufficiency reduces the reactivity of the cardiovascular system to sympathetic stimulation (Ramey & Goldstein, 1957); a degree of cortical insufficiency in demedullated rats may explain the reduced pressor response to splanchnic stimulation in these animals.…”

“…Thus adrenal demedullation by expression is followed by a fall in the urinary excretion of adrenaline which is similar to that observed after adrenal demedullation with cortical grafting (Del Basso, Rusca & Carpi, 1967). During a phase of sympathetic hyperactivity, an increase in adrenaline excretion is observed in rats demedullated by expression (Biscardi, Carpi & Orsingher, 1964) whereas it is absent in rats demedullated with cortical grafting (Del Basso, Rusca & Carpi, 1967).…”

General Pharmacology of Amphetamine-Like Drugs

“…An increase in the urinary excretion of NA and adrenaline in the rat after acute amphetamine administration has been demonstrated (BISCARDI et al, 1964;BEAU-VALLETet al, 1966b;GUNNE and LEWANDER, 1967;LEWANDER, 1968a, b;BEAUVAL-LET, 1968;BASSO et al, 1970). The ganglion blocking agent, mecamylamine, blocked the effect of amphetamine on the NA excretion but not on the A excretion; adrenal demedullation (by expression) did not completely block the increase in the A excretion after amphetamine (BISCARDI et al, 1964).…”

Maintenance of Noradrenaline Synthesis in Rats after Reserpine Treatment

“…Rats used for studying reserpine influence on urinary excretion of NA and VMA were bilaterally adrenodemedullated according to Biscardi, Carpi and Orsinger (1964). Urine collection was initiated 5-12 days after the surgery.…”