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1 Department of Pharmacology, College of Medicine, The University of Iowa, Iowa City, Iowa
The effect of furosemide on renal hemodynamics has been studied quite extensively. However, the possibility that the hemodynamic effects of furosemide are not limited to renal vessels and that this drug also affects other vascular beds has not been examined. In the present study the effect of furosemide on limb blood flow was assessed in unanesthetized dogs containing chronically implanted flow transducers and pressure cannulas. The results showed that the effect of flurosemide on limb blood flow differs quite markedly from the effect of this drug on renal blood flow. Furosemide increases renal blood flow but was found to produce a decrease in limb blood flow. Renal blood flow rose rapidly after drug administration, was elevated maximally by 10 minutes and had returned to the control level of flow by 30 minutes after drug administration. Limb blood flow, in contrast, decreased much less rapidly and remained below the control level of flow after reqal blood flow had returned to the control level of flow. Intraiiac infusions of furosemide failed to alter limb blood flow; whereas, intrarenal infusions of the drug produced almost immediate changes in renal blood flow. Changes in renal blood flow and limb blood flow produced by furosemide were not altered by prior treatment with the ganghionic blocking agent pentolinium. Thus, furosemide does not appear to act directly on limb vascular smooth muscle nor does it appear to decrease limb blood flow by an indirect neurogenic or reflex mechanism. However, when furosemide was given to nephrectomized dogs, it was found that bilateral nephrectomy abolished the decrease in limb blood flow produced by furosemide. It therefore appears that the sustained decrease in limb blood flow produced by furosemide administration may result from the action of a circulating vasoconstrictor substance elaborated by the kidney.
Submitted on August 8, 1969