Cause of genuine autoregulation of the renal circulation.

I T HAS long been known that one of the most striking features of the normal renal circulation is its autonomous capacity to change its resistance in the face of changed arterial pressure, so that renal blood flow stays relatively constant.' 2 Ever since, there has been much question as to whether this renal circulatory autoregulation is caused by a vital vasomotor response or by a passive physical mechanism. The strongest evidence that renal autoregulation may involve a mechanical response rather than one of active vasomotion is that of Winton,' 5 who reported autoregulation of blood flow in isolated kidneys cooled to 3 to 12 C. and in kidneys poisoned with chloral hydrate. Recent work by Hinshaw and associates' and by Scher supports this theory, for their data suggest that the changed resistance underlying autoregulation is caused by compression of vascular channels by altered interstitial pressure. Kinter and Pappenheimer also believed that renal autoregulation was a passive physical phenomenon but attributed it to increased viscous resistance of cell-rich blood due to intrarenal plasma skimming. They, as well as others,' n did not find autoregulation in kidneys perfused with cell-free colloidal solutions.