Endothelium-dependent vasodilation is mediated by nitric oxide (NO), prostaglandins (PG), and endothelium-derived hyperpolarizing factor (EDHF). We studied the contributions and temporal characteristics of these components in the renal vasodilator responses to acetylcholine (ACh) and bradykinin (BK) and in the buffering of vasoconstrictor responses to norepinephrine (NE) and angiotensin II (Ang II). Renal blood flow (RBF) and vascular conductance (RVC) were studied in anesthetized rats in response to renal arterial bolus injections before and after inhibition of NO-synthase (LNAME), cyclooxygenase (indomethacin, INDO), or both. ACh increased RVC peaking at tmax=29s. LNAME (n=8) diminished the integrated response, and made it substantially faster (tmax=18s). The point-by-point difference caused by LNAME (=NO component) integrated to 74% of control and was much slower (tmax=38s). INDO (n=9) reduced the response without affecting tmax (36 vs. 30s). The difference (=PG) reached 21% of the control with tmax=25s. LNAME+INDO (n=17) reduced the response to 18% and markedly accelerated tmax to 16s (=EDHF). Results were similar for BK with slightly more PG- and less NO-contribution than for ACh. Constrictor responses to NE and AngII were augmented and decelerated by LNAME and LNAME+INDO. The calculated difference (=buffering by NO or NO+PG) was slower than the constriction. It is concluded that NO, PG, and EDHF contribute >50%, 20-40%, and <20% to the renal vasodilator effect of ACh and BK. EDHF acts substantially faster and less sustained (tmax=16s) than NO and PG (tmax=30s). Constrictor buffering by NO and PG is not constant over time, but renders the constriction less sustained.