Angiotensin I decreases renal blood flow and increases renal vascular resistance primarily through its intrarenal conversion to angiotensin II.
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Intrarenal angiotensin conversion appears limited in this model; leaves open its quantitative role in human renal hemodynamics.
Effects of close intra-arterial injections of angiotensins I and II on changes in renal blood flow and renal vascular resistance were studied in dogs anesthetized with pentobarbital sodium. In the first series of experiments, angiotensin I (0.375 µg) or angiotensin II (0.13 µg) decreased renal blood flow and pressures in a small renal cortical vein and the renal vein. Although renal vascular resistance was markedly increased by angiotensins I or II, these increases did not appear to involve renal venous segments. Responses to angiotensin I occurred when the injected agonist was not allowed to reach the systemic circulation, and were virtually abolished during infusion of SQ 20475, a synthetic pentapeptide (Pyr-Lys-Try-Ala-Pro) that inhibits enzymatic conversion of angiotensin I to angiotensin II. In the second series of experiments, renal vascular responses to intra-arterial injections of angiotensin I (0.375-3.75 µg) and angiotensin II (0.13-1.00 µg) were studied. Responses to angiotensin I, but not those to angiotensin II, were significantly attenuated by SQ 20475. The results suggest that similar renal vascular segments respond to angiotensins I and II. Responses to angiotensin I are probably due to its intrarenal conversion to angiotensin II. Such conversion appears to occur to the extent of about 4%.
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Salvo et al. (1971) studied this question.
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