Johnson J A, Kurz K D, Siripaisarnpipat S, Koivunen D G, Zeigler D W, Sakamaki T, Payne C G
Hypertension. 1983 Jul-Aug;5(4):453-9. doi: 10.1161/01.hyp.5.4.453.
Prehypertensive rabbits with renal artery stenosis of 3 days' duration (one-kidney, one clip) are known to have increased pressor responses to norepinephrine and vasopressin; this pressor hyperresponsiveness is restored to normal by the angiotensin II (AII) antagonist, [ Sar1, Ile8 ] AII, even though plasma renin activity (PRA) and plasma AII concentrations are not elevated. In the present study, the cross-circulation of blood between conscious one-kidney, 3-day renal artery stenosis rabbits and conscious normal rabbits resulted in the transfer of pressor hyperresponsiveness to the normal rabbits, although both groups of rabbits had normal values for PRA. A similar cross-circulation of blood between one-kidney rabbits without renal artery stenosis and normal rabbits did not alter the pressor responsiveness of the normal rabbits to norepinephrine. It was concluded that a circulating humoral factor is involved in mediating pressor hyperresponsiveness in 3-day renal artery stenosis rabbits. To evaluate the interrelationship between AII and the hormonal hyperresponsiveness factor, an additional experiment was performed in which blood was cross-circulated between one-kidney, 3-day renal artery stenosis rabbits and normal rabbits, with the normal rabbits receiving [ Sar1, Ile8 ] AII immediately following cross-circulation. Administration of this AII antagonist to the normal rabbits prevented them from showing pressor hyperresponsiveness following the cross-circulation of blood. It is concluded that in this prehypertensive renal artery stenosis model the humoral hyperresponsiveness factor exerts its effect through AII mechanisms, rather than AII acting to increase the release or secretion of the hyperresponsiveness factor.
已知患有持续3天肾动脉狭窄(一侧肾,一个夹子)的高血压前期兔子对去甲肾上腺素和血管加压素的升压反应增强;即使血浆肾素活性(PRA)和血浆血管紧张素II(AII)浓度未升高,这种升压反应性增高也可通过血管紧张素II(AII)拮抗剂[ Sar1,Ile8 ] AII恢复正常。在本研究中,有意识的一侧肾、3天肾动脉狭窄兔子与有意识的正常兔子之间进行血液交叉循环,导致升压反应性增高转移至正常兔子,尽管两组兔子的PRA值均正常。一侧肾无肾动脉狭窄的兔子与正常兔子之间进行类似的血液交叉循环,并未改变正常兔子对去甲肾上腺素的升压反应性。得出的结论是,一种循环体液因子参与介导3天肾动脉狭窄兔子的升压反应性增高。为了评估AII与激素反应性增高因子之间的相互关系,进行了另一项实验,即一侧肾、3天肾动脉狭窄兔子与正常兔子之间进行血液交叉循环,正常兔子在交叉循环后立即接受[ Sar1,Ile8 ] AII。给正常兔子施用这种AII拮抗剂可防止它们在血液交叉循环后出现升压反应性增高。得出的结论是,在这个高血压前期肾动脉狭窄模型中,体液反应性增高因子通过AII机制发挥作用,而不是AII作用于增加反应性增高因子的释放或分泌。