To investigate whether alpha-adrenergic mechanisms would participate in the vascular response to normothermic or hypothermic perfusion of the isolated rat kidney, four groups of rats were studied. They were perfused for 15 min at 37 degrees C with either normal saline (group I) or prazosin (group II) or at 32 degrees C with saline (group III) or prazosin (group IV). Both in group I and in group III perfusate flow tended to fall with time, although this was significant in group I only. In group II prazosin prevented the drop in flow rates; in group IV this drug even increased flow. At all times flow rates in group IV were significantly higher than in group II. It is concluded that at normothermic perfusion an alpha-adrenergic mechanism is activated that slowly constricts the renal vessels. At 32 degrees C intense alpha-adrenergic vasoconstriction occurs; enhanced flow rates at this temperature may be explained by shunting through intrarenal arteriovenous anastomoses.
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