Mackay I G, Macnicol A M, Smith H J, Cumming A D, Watson M L
Br J Clin Pharmacol. 1985 Sep;20(3):197-203. doi: 10.1111/j.1365-2125.1985.tb05061.x.
The effects of a 21 infusion of isotonic sodium chloride on renal haemodynamics and sodium excretion were measured in nine normotensive volunteers. Changes in these responses to volume expansion induced by cardioselective beta-adrenoceptor blockade by drugs with (epanolol) and without intrinsic sympathomimetic activity (atenolol) were examined. Renal plasma flow was significantly lower before, during and after sodium chloride infusion whilst on treatment with atenolol compared with epanolol. Urinary sodium excretion was lower on atenolol than epanolol. Glomerular filtration rate was unchanged by either drug. Basal urinary kallikrein excretion was diminished by atenolol and both epanolol and atenolol inhibited the rise in urinary kallikrein excretion after sodium chloride infusion. Although some of these findings may be due to a more potent hypotensive effect of atenolol, intrinsic sympathomimetic activity may contribute to the apparent protective effects of epanolol on renal function.
在9名血压正常的志愿者中,测量了等渗氯化钠21小时输注对肾脏血流动力学和钠排泄的影响。研究了使用具有(依泮洛尔)和不具有内在拟交感活性(阿替洛尔)的药物进行心脏选择性β-肾上腺素能受体阻滞所诱导的容量扩张对这些反应的变化。与依泮洛尔相比,在使用阿替洛尔治疗期间及之后,输注氯化钠之前、期间和之后的肾血浆流量显著降低。阿替洛尔治疗时的尿钠排泄低于依泮洛尔。两种药物均未改变肾小球滤过率。阿替洛尔使基础尿激肽释放酶排泄减少,依泮洛尔和阿替洛尔均抑制了输注氯化钠后尿激肽释放酶排泄的增加。尽管其中一些发现可能归因于阿替洛尔更强的降压作用,但内在拟交感活性可能有助于依泮洛尔对肾功能的明显保护作用。