1. The relative ability of the renal and femoral vascular beds to remove infused angiotensin II and noradrenaline was examined in anaesthetized greyhounds.

2. The degree of extraction of infused drug by each vascular bed was expressed as a percentage, calculated by comparing the pressor response to intra-arterial infusion with that obtained when the same dose was administered by the intravenous route.

3. When compared with the same dose given intravenously, the pressor responses after renal artery administration of angiotensin II were reduced by a mean of 77·8 ± 4·1% (mean ± sem, n = 12), whereas those after femoral artery infusions at the same dose were reduced by a mean of only 27·2 ± 4·9%(n = 12).

4. The pattern of extraction seen with noradrenaline infusions administered in a similar manner was the reverse of that with angiotensin II. There was a 28·9 ± 6·8% (n = 7) reduction in pressor responses to renal artery infusions; in contrast, femoral artery infusions of the same dose exhibited a 99·0 ± 1·0% (n = 7) reduction in the pressor responses.

5. Local arterial administration of the angiotensin II competitive antagonist, [Sar1,Ile8]angiotensin II, potentiated the systemic pressor responses to renal artery infusions of angiotensin II, but not those to femoral artery infusions.

6. It is suggested that the marked ability of the renal vascular bed to remove circulating angiotensin II may, in part, involve receptor-binding, although this seems not to be the case in the femoral vascular bed.

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