The effect on the electrolyte balance of a dopaminergic agonist (bromocriptine) and an antagonist (metoclopramide) and their effect on renal aldosterone and kallikrein excretion were investigated. Ten normotensive Wistar rats and ten spontaneously hypertensive rats (SHR-Wistar Kioto) were treated with BCR (4 mg/Kg weight b.i.d.) for 4 days; after a week of pharmacological wash-out they received MCP (0,5 mg/Kg weight b.i.d.) for 4 days. Before and after treatment and at the 2nd and 4th day of each treatment diuresis, urinary excretion of aldosterone, kallikrein, sodium, potassium and proteins were measured. During the 24-hour urine collections the rats were kept in separate metabolic cages with free access to food and water. Kallikrein urinary excretion was lower in SHR than in normotensive rats under basal conditions (p 0.05); urinary sodium, potassium, proteins and sodium/potassium rate were also reduced in SHR. After treatment with bromocriptine a further reduction in urinary kallikrein excretion was observed in SHR. After MCP all the parameters were unchanged both in normotensive rats and in SHR, but SHR showed a significant correlation between aldosterone and kallikrein excretion (p less than 0,001); in this condition it seems that in SHR the control exerted by aldosterone on kallikrein excretion is greater than the one exerted by dopamine. It may indicate a defect of the natriuretic and vasodilator dopaminergic system in spontaneously hypertensive rats.
[The effect of dopaminergic stimulation and inhibition on the urinary excretion of aldosterone and kallikrein in spontaneously hypertensive rats]
MINUZ, Pietro;SANTONASTASO, Clara;DELVA, Pietro;LECHI, Alessandro
1983-01-01
Abstract
The effect on the electrolyte balance of a dopaminergic agonist (bromocriptine) and an antagonist (metoclopramide) and their effect on renal aldosterone and kallikrein excretion were investigated. Ten normotensive Wistar rats and ten spontaneously hypertensive rats (SHR-Wistar Kioto) were treated with BCR (4 mg/Kg weight b.i.d.) for 4 days; after a week of pharmacological wash-out they received MCP (0,5 mg/Kg weight b.i.d.) for 4 days. Before and after treatment and at the 2nd and 4th day of each treatment diuresis, urinary excretion of aldosterone, kallikrein, sodium, potassium and proteins were measured. During the 24-hour urine collections the rats were kept in separate metabolic cages with free access to food and water. Kallikrein urinary excretion was lower in SHR than in normotensive rats under basal conditions (p 0.05); urinary sodium, potassium, proteins and sodium/potassium rate were also reduced in SHR. After treatment with bromocriptine a further reduction in urinary kallikrein excretion was observed in SHR. After MCP all the parameters were unchanged both in normotensive rats and in SHR, but SHR showed a significant correlation between aldosterone and kallikrein excretion (p less than 0,001); in this condition it seems that in SHR the control exerted by aldosterone on kallikrein excretion is greater than the one exerted by dopamine. It may indicate a defect of the natriuretic and vasodilator dopaminergic system in spontaneously hypertensive rats.
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