Imbs J L, Schmidt M, Giesen E M, Schwartz J
J Physiol (Paris). 1984;79(6):481-4.
Renin release elicited by i.v. injection of loop-diuretics was used to study the effects of angiotensin II (AII) on intrarenal hemodynamics. The vasoconstrictive action of intrarenally synthesized AII predominates in the efferent glomerular arteriole. Such a vasoconstrictive effect could affect blood flow in the vasa recta which stem from efferent arterioles of juxtamedullary glomeruli. Renin secretion and renal inner medullary blood flow (tissue clearance of 133Xe) were simultaneously measured before and after frusemide-induced renin release. The relationship between renin secretion and renal inner medullary blood flow was inverse. Changes in renal medullary blood flow may be physiological determinants of medullary osmolality and renal concentration ability. The intrarenal role of AII in urinary concentration recovery after frusemide was examined. Inhibition of renin release by propranolol or AII-blockade (by saralasin or Hoe 409) delayed recovery of urinary osmolality. In the conscious rat, propranolol slowed down recovery of the cortico-papillary gradient for sodium. Its vasoconstrictive action on the efferent glomerular arteriole might enable the renin-angiotensin system to participate in the control of renal excretion of salt and water.
通过静脉注射袢利尿剂引发肾素释放，以此研究血管紧张素II（AII）对肾内血流动力学的影响。肾内合成的AII的血管收缩作用在出球小动脉中占主导。这种血管收缩效应可能会影响源自近髓肾单位出球小动脉的直小血管中的血流。在速尿诱导肾素释放前后，同时测量肾素分泌和肾内髓质血流（133Xe的组织清除率）。肾素分泌与肾内髓质血流之间呈负相关。肾髓质血流的变化可能是髓质渗透压和肾脏浓缩能力的生理决定因素。研究了AII在速尿后尿浓缩恢复中的肾内作用。普萘洛尔抑制肾素释放或AII阻断（通过沙拉新或Hoe 409）会延迟尿渗透压的恢复。在清醒大鼠中，普萘洛尔减缓了皮质 - 乳头钠梯度的恢复。其对出球小动脉的血管收缩作用可能使肾素 - 血管紧张素系统参与对肾脏盐和水排泄的控制。
