Abstract
It is generally agreed that the hypertension which develops in experimental animals as a result of partial 1 or complete 2 ischemia of the kidneys is of humoral and not of nervous origin.
Although renin, a pressor extract prepared from the renal cortex, has been implicated by some observers, 3 , 4 neither this product nor any other has to date been proved to be the substance responsible for ischemic hypertension.
In this communication we wish to report the rinding of a per-fusate of ischemic kidneys which causes the elevation of blood pressure following the release of complete renal ischemia. Until the precise nature of the active principle has been determined, we propose the name ischemin, which may be defined as the pressor substance contained in perfusates of completely ischemic kidneys and which is responsible for the hypertension resulting from the release of total renal ischemia. For convenience, the renal per-fusate containing the pressor substance will also be termed ischemin.
The results of the observations made thus far are summarized briefly.
In 8 experiments, cats were anesthetized with ether and the renal pedicle of one kidney clamped. After 4 to 6 hours the animal was reanesthetized with nembutal, the blood pressure recorded from the carotid artery, and both the normal and ischemic kidneys removed. Within 5 minutes following the removal of the kidneys, both renal arteries were cannulated and the kidneys perfused with 1 cc of warm saline per gram of kidney. The perfusates were then injected intravenously into the same animal. The perfusates of the ischemic kidneys uniformly gave a marked and prolonged rise in blood pressure, amounting to as much as 100 mm of Hg, whereas those obtained from the normal kidneys had no pressor effect.
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