Blockade of postocclusive renal vasoconstriction by an angiotensin II antagonists: evidence for an angiotensin-adenosine interaction

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Abstract
In contrast to the reactive hyperemia of most tissues, the kidney demonstrates a postocclusive vasoconstriction. This vasoconstriction was attributed to the intrarenal accumulation of adenosine, which is vasoconstrictive in the kidney and is known to increase during renal ischemia. The effects of a competitive angiotensin II (AII) antagonist ([Sar1, Ile]AII) on the vasoconstrictive response to adenosine and the postocclusive vasoconstriction were studied. In 6 Na-depleted dogs, single intrarenal injections of adenosine (1-100 nmol) produced a dose-related decrease in renal blood flow. Simultaneous infusion of [Sar1,Ile8]AII at 3 .mu.g/kg per min had no effect on the adenosine dose-response curve. When [SAR1,Ile8]AII was increased to 15 and 50 .mu.g/kg per min the vasoconstrictive response to adenosine was attenuated in a dose-related manner. In 5 meclofenamate-treated Na-depleted dogs, occlusion of the renal artery (5-60 s) produced a time-related vasoconstrictive response. Simultaneous intrarenal infusion of [Sar1,Ile8]AII at a dose sufficient to block circulating AII (3 .mu.g/kg per min) did not have any substantial effect on the response. When the [Sar1,Ile8]AII was infused at 50 .mu.g/kg per min, which had no additional effect on renal hemodynamics, the postocclusive vasoconstriction was markedly attenuated. Apparently the intrarenal vasoconstriction of adenosine is mediated by an angiotensin mechanism, and the renal postocclusive vasoconstriction may be due to an adenosine-angiotensin interaction.

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