The prostaglandins comprise a large family of substances that includes primary prostaglandins (PGE2, F2 alpha, D2) prostacyclin (PGI2), and thromboxanes (TxA2, B2), all of which exhibit some vascular activity. The activity of each prostaglandin may be species- and organ-dependent, and the type of prostaglandin produced in a tissue is often dependent on the presence of terminal enzyme systems in that tissue. This paper describes the effects of certain members of the prostaglandin family on the mesenteric and renal vascular beds of anesthetized dogs. In the kidney, arachidonic acid, PGE2, D2, and I2 all produce vasodilation when studied by bolus injection techniques. PGF2 alpha is relatively inactive. In the mesenteric vascular bed arachidonate, PGE2 and PGI2 are vasodilators whereas PGD2 and PGF2 are vasoconstrictors. The direct actions of thromboxanes A2 and the endoperoxide PGH2 are uncertain because of their very short half-lives in plasma. Infusion of prostaglandins E2 and I2 into the left ventricle produces vasodilation in both the kidney and the gut. In the mesenteric vascular bed, however, vasodilation during PGE2 (but not PGI2) infusion is a transient phenomenon and the blood flow returns to control levels within the first few minutes of infusion. The vascular actions of prostaglandins are therefore complex and are dependent not only on organ and species, but on experimental technique as well.