Minuz P, Gangi F, Degan M, Lechi C, Delva P, Lechi A
Boll Soc Ital Biol Sper. 1983 Oct 30;59(10):1435-41.
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.
研究了多巴胺能激动剂(溴隐亭)和拮抗剂(甲氧氯普胺)对电解质平衡的影响及其对肾醛固酮和激肽释放酶排泄的影响。十只血压正常的Wistar大鼠和十只自发性高血压大鼠(SHR-Wistar Kioto)接受溴隐亭(4mg/kg体重,每日两次)治疗4天;在经过一周的药物洗脱期后,它们接受甲氧氯普胺(0.5mg/kg体重,每日两次)治疗4天。在治疗前后以及每种治疗的第2天和第4天,测量尿量、醛固酮、激肽释放酶、钠、钾和蛋白质的尿排泄量。在24小时尿液收集期间,将大鼠置于单独的代谢笼中,可自由获取食物和水。在基础条件下,SHR的尿激肽释放酶排泄量低于血压正常的大鼠(p<0.05);SHR的尿钠、钾、蛋白质和钠/钾比率也降低。用溴隐亭治疗后,SHR的尿激肽释放酶排泄量进一步降低。在用甲氧氯普胺治疗后,血压正常的大鼠和SHR的所有参数均未改变,但SHR的醛固酮和激肽释放酶排泄之间存在显著相关性(p<0.001);在这种情况下,似乎在SHR中醛固酮对激肽释放酶排泄的控制作用大于多巴胺的控制作用。这可能表明自发性高血压大鼠中利钠和血管舒张多巴胺能系统存在缺陷。