Susić D, Radujković-Kuburović G, Jerkić M, Jovović D, Varagić J, Vukobratović S, Veljković V
Institute for Medical Research, Belgrade, Yugoslavia.
Indian J Med Res. 1995 Aug;102:81-5.
To examine whether changes in renomedullary osmolality and the activity of the renin-angiotensin system may influence the ability of the renal medulla to exert an antihypertensive function, rats were exposed to several manoeuvers. These affected either the medullary osmolality or the renin-angiotensin system (salt or saccharose load, salt depletion, treatment with captopril alone or in combination with salt depletion). A comparison of the antihypertensive capacity of the renal medulla was studied by transplanting renal medullae from the various groups into one-kidney one-clip hypertensive rats. A significant and quantitatively similar reduction in blood pressure was observed in hypertensive rats that received transplants of the medullae from control, salt or saccharose loaded rats and captopril treated rats. In contrast, medullae from salt depleted rats did not affect blood pressure when transplanted into hypertensive animals. The addition of captopril restored the antihypertensive function of renal medulla in salt depleted rats. The results do not support the view that osmolality of the renal medulla regulates its antihypertensive capacity, and suggest that angiotensin II may restrain renomedullary antihypertensive function.
为了研究肾髓质渗透压和肾素 - 血管紧张素系统活性的变化是否会影响肾髓质发挥降压功能的能力,对大鼠进行了多种操作。这些操作分别影响髓质渗透压或肾素 - 血管紧张素系统(盐或蔗糖负荷、盐耗竭、单独使用卡托普利或与盐耗竭联合治疗)。通过将不同组的肾髓质移植到单肾单夹高血压大鼠体内,研究了肾髓质的降压能力。在接受来自对照、盐或蔗糖负荷大鼠以及卡托普利治疗大鼠的髓质移植的高血压大鼠中,观察到血压有显著且数量上相似的降低。相比之下,将盐耗竭大鼠的髓质移植到高血压动物体内时,对血压没有影响。添加卡托普利可恢复盐耗竭大鼠肾髓质的降压功能。结果不支持肾髓质渗透压调节其降压能力的观点,并表明血管紧张素 II 可能抑制肾髓质的降压功能。