VandenBurg M J, Sharman V L, Morton J J, Williams G H, Marsh F P
Postgrad Med J. 1981 May;57(667):283-8. doi: 10.1136/pgmj.57.667.283.
Changes induced by i.v. and subcutaneous teprotide in plasma renin, angiotensin I, angiotensin II, aldosterone and bradykinin were studied in a renal transplant patient with severe high renin hypertension, before and after trinephrectomy. The immediate reduction in BP produced by teprotide was not solely attributable to the inhibition of conversion of angiotensin I to angiotensin II, because there was also a transient increase in serum bradykinin; however, the prolonged antihypertensive effect of teprotide appeared independent of bradykinin. After trinephrectomy, teprotide lowered systolic BP but had no significant effect on diastolic BP or plasma bradykinin. beta-Blockade prevented the secondary increase in plasma renin which followed teprotide, thereby potentiating its anti-hypertensive effect.
在一位患有严重高肾素性高血压的肾移植患者中，研究了静脉注射和皮下注射替普罗肽对血浆肾素、血管紧张素I、血管紧张素II、醛固酮和缓激肽的影响，观察时间为三肾切除术前和术后。替普罗肽引起的血压立即下降并非仅归因于对血管紧张素I向血管紧张素II转化的抑制，因为血清缓激肽也有短暂升高；然而，替普罗肽的长期降压作用似乎与缓激肽无关。三肾切除术后，替普罗肽降低了收缩压，但对舒张压或血浆缓激肽无显著影响。β受体阻滞剂可防止替普罗肽后血浆肾素的继发性升高，从而增强其降压作用。
