Mitchell H C, Keeton T K, Pettinger W A
Kidney Int Suppl. 1979 Mar(9):S101-6.
Diuretic and vasodilator drugs alter the BP response to saralasin causing drug interactions. Saralasin-induced BP reduction is related directly to PRA and intravascular volume. Diuretic agents deplete intravascular volume and elevate PRA, enhancing saralasin hypotension. Vasodilating agents increase PRA and may induce angiotensin dependence of BP. Thus, with potent vasodilators, saralasin can induce hypotension. Rebound hypertension has been reported after saralasin infusion in several patients with accelerated or malignant hypertension. Theoretically, this BP elevation could be related to sustained release of renin resulting from disinhibition of an intrarenal angiotensin receptor inhibitory to renin release. Since propranolol can block saralasin-induced renin release, angiotensin and beta-blockers could constitute a beneficial drug interaction.
利尿剂和血管扩张剂会改变血压对沙拉新的反应,从而导致药物相互作用。沙拉新引起的血压降低与肾素活性(PRA)和血管内容量直接相关。利尿剂会消耗血管内容量并升高PRA,增强沙拉新的降压作用。血管扩张剂会增加PRA,并可能导致血压对血管紧张素产生依赖性。因此,使用强效血管扩张剂时,沙拉新可诱发低血压。据报道,在数例急进性或恶性高血压患者中,输注沙拉新后出现了血压反跳升高。从理论上讲,这种血压升高可能与肾内血管紧张素受体对肾素释放的抑制作用解除后肾素的持续释放有关。由于普萘洛尔可阻断沙拉新诱导的肾素释放,血管紧张素和β受体阻滞剂可能构成有益的药物相互作用。