Hanson R C, Davis J O, Freeman R H
Proc Soc Exp Biol Med. 1976 Jun;152(2):224-8. doi: 10.3181/00379727-152-39366.
Dogs were given d,1-propranolol before and after thoracic inferior vena cava constriction (TIVCC) or renal artery constriction (RAC) to determine if the increase in plasma renin activity (PRA) and associated biological activity could be suppressed. Oral propranolol administration (240 mg twice daily) was begun at least 2 days prior to TIVCC in six dogs; heart rate was reduced from 133 to 95 beats/min but PRA did not change with propranolol administration. After TIVCC and during continued propranolol administration, daily renal sodium excretion fell from an average value of 50 to less than 3 mEq sodium/day and PRA was elevated two- to fourfold. With prolonged propranolol administration during TIVCC, PRA returned toward normal levels but renal sodium excretion remained low. At this time, hourly measurements of sodium excretion showed no change after a 240-mg oral dose or propranolol although very high plasma levels of propranolol were achieved; also, PRA was unchanged and low. The effects of RAC were studied before and during an intravenous propranolol infusion (0.2 mg/kg/hour) in conscious animals. Before propranolol administration, arterial pressure increased during RAC from 120 to 136 mm Hg and PRA doubled. Propranolol infusion lowered heart rate from 110 to 84 beats/min, but arterial pressure and PRA were not attentuated by propranolol during RAC. The data indicate that non-beta-adrenergic mechanisms are involved in renin release during TIVCC and RAC.
在犬进行胸段下腔静脉缩窄（TIVCC）或肾动脉缩窄（RAC）之前和之后给予消旋普萘洛尔，以确定血浆肾素活性（PRA）的升高及相关生物活性是否能够被抑制。在6只犬进行TIVCC前至少2天开始口服普萘洛尔（每日2次，每次240 mg）；心率从133次/分钟降至95次/分钟，但给予普萘洛尔后PRA未发生变化。在TIVCC后并持续给予普萘洛尔期间，每日肾钠排泄量从平均50 mEq钠/天降至不足3 mEq钠/天，且PRA升高了2至4倍。在TIVCC期间长期给予普萘洛尔，PRA恢复至正常水平，但肾钠排泄量仍维持在低水平。此时，每小时测量钠排泄量显示，口服240 mg普萘洛尔后无变化，尽管普萘洛尔血浆水平非常高；同样，PRA未改变且处于低水平。在清醒动物静脉输注普萘洛尔（0.2 mg/kg/小时）之前和期间研究了RAC的作用。在给予普萘洛尔之前，RAC期间动脉压从120 mmHg升至136 mmHg，PRA翻倍。输注普萘洛尔使心率从110次/分钟降至84次/分钟，但在RAC期间普萘洛尔未减弱动脉压和PRA。数据表明，非β-肾上腺素能机制参与了TIVCC和RAC期间的肾素释放。
