Puri V N, Sur R N
Acta Pharmacol Toxicol (Copenh). 1985 Feb;56(2):91-3. doi: 10.1111/j.1600-0773.1985.tb01259.x.
In male Charles Foster rats, intracerebroventricular clonidine (0.2, 1.0, 10 mmol/l) caused dose dependent increase in the urine output and sodium excretion (P less than 0.01). Urinary creatinine excretion was decreased to a significant level (P less than 0.02). Urinary potassium excretion was increased but was not dose dependent. Maximal increase in the urine volume occurred during first hour of clonidine administration. Intraperitoneal administration of clonidine in similar molar concentration failed to produce changes in the urine volume. The results indicate that clonidine-induced diuresis is centrogenic and is attributed to the inhibition of the release of vasopressin from central hypothalamoneurohypophyseal axis.
在雄性查尔斯·福斯特大鼠中,脑室内注射可乐定(0.2、1.0、10 mmol/l)可导致尿量和钠排泄量呈剂量依赖性增加(P<0.01)。尿肌酐排泄量显著降低(P<0.02)。尿钾排泄量增加,但不呈剂量依赖性。可乐定给药后第一小时尿量增加最大。腹腔注射相同摩尔浓度的可乐定未能引起尿量变化。结果表明,可乐定诱导的利尿作用是中枢性的,归因于对下丘脑神经垂体轴中央释放血管加压素的抑制。