Hollenberg N K, Adams D F, McKinstry D N, Williams G H, Borucki L J, Sullivan J M
Br J Clin Pharmacol. 1979;7 Suppl 2(Suppl 2):219S-225S. doi: 10.1111/j.1365-2125.1979.tb04693.x.
1 Nadolol was administered intravenously to five hypertensive patients and three healthy volunteers in balance on a 10 mEq sodium intake. 2 Nadolol (0.3-10.0 micrograms/kg) induced a significant, dose-related increase in renal blood flow, measured with radioxenon, with a maximum increase of 72 +/- 4 ml/100g/min (26%) at 3.0 micrograms/kg. 3 Heart rate and plasma renin activity decreased significantly over the same dose range. 4 The renal vascular response to nadolol contrasts sharply with those found with other beta-adrenoceptor-blocking agents. 5 The magnitude of the increase in renal blood flow, its time-course and the parallel fall in plasma renin activity raise the possibility that the renal vasodilation reflects the reversal of angiotensin's influence on the renal arterial bed.
给五名高血压患者和三名健康志愿者静脉注射纳多洛尔,他们的钠摄入量均为10毫当量以保持平衡。
纳多洛尔(0.3 - 10.0微克/千克)可使通过放射性氙测定的肾血流量显著增加,且呈剂量相关性,在3.0微克/千克时最大增加量为72±4毫升/100克/分钟(26%)。
在相同剂量范围内,心率和血浆肾素活性显著降低。
纳多洛尔对肾血管的反应与其他β-肾上腺素能受体阻滞剂的反应形成鲜明对比。
肾血流量增加的幅度、其时间进程以及血浆肾素活性的平行下降增加了肾血管舒张反映血管紧张素对肾动脉床影响逆转的可能性。