Abstract
THE parenteral administration of saline extracts of renal tissue to nephrectomized animals of various species causes protracted elevation of blood pressure, increased drinking, formation of ascites and pleural effusions, and arteriolar necrosis1–7. While renin has been implicated in pathogenesis as it is a major component of saline renal extracts, the mechanisms producing these various phenomena and their interrelationship remain unclear. It has been postulated5,6 that the blood pressure response is due to angiotensin II generated by the renin-rich extract and the effusions caused by changes in vascular permeability induced by the blood pressure elevation. Asscher7, however, suggested that another factor of renal origin was involved which increased vascular permeability to plasma proteins.
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