A B S T R A C T The mechanism whereby the vasoconstrictor response to angiotensin II (A,,) is influenced by sodium balance or disease is unclear. To explore this question, the renal vascular responses (RVR) to intrarenal injections of subpressor doses of A,, and norepinephrine were studied in dogs with an electromagnetic flowmeter. Acute and chronic sodium depletion increased plasma renin activity (PRA) and blunted the RVR to A,,, while acute sodium repletion and chronic sodium excess plus desoxycorticosterone acetate decreased PRA and enhanced the RVR to All.The magnitude of the RVR to Al1 was inversely related to PRA. The RVR to norepinephrine was unaffected by sodium balance and was not related to PRA. Inhibition of the conversion of angiotensin I to Al, by SQ 20,881 during sodium depletion lowered mean arterial blood pressure (MABP), increased renal blood flow (RBF), and enhanced the RVR to Al, but not to norepinephrine. Administration of bradykinin to chronically sodium-depleted dogs also lowered the MABP and increased RBF but had no effect on the RVR to A11. SQ 20,881 had no effect on MABP, RBF, or the RVR to Al1 in the dogs with chronic sodiuni excess and desoxycorticosterone acetate. Administration of indomethacin to chronically sodium-depleted dogs lowered RBF but did not influence the RVR to A,,.The results indicate that the RVR to A,, is selectively influenced by sodium balance and that the magnitude of the response is inversely related to the availability of endogenous AII The data did not suggest that the variations in the RVR to A,, were because of direct effects of sodium on vascular contraction, changes in