Ascorbate reduces the oxidation rate of catecholamines, and by an independent mechanism enhances rabbit aortic ring contractions initiated by catecholamines. The largest significantly different fractional increases in force produced by ascorbate enhancement of norepinephrine (NE), epinephrine, phenylpropanolamine (PPA) and ephedrine (EPH) are 5.5, 1.8, 1.6 and 1.3 times, respectively. NE, PPA and EPH have oxidation rate constants in physiological salt solutions bubbled with 95% oxygen at 37C of 1.24, 247 and 643 hours, respectively. Ascorbate significantly enhances 100 nM NE contractions by 2-fold or greater at all ascorbate concentrations greater than 15 microM, including the entire physiological range 40-100 microM. Ascorbate preloading and washout followed by NE exposure produces significantly greater contractions than NE without ascorbate preloading, but significantly lower than contractions in which ascorbate and NE are present simultaneously. Ascorbate does not enhance potassium-induced or angiotensin II-induced contractions. Ascorbate enhancement of catecholamine contractions occurs in addition to the reduction in oxidation rate because: the increases in force occur faster than oxidation can occur; the increases occur with compounds that have negligible oxidation rates; and the increases occur when ascorbate and NE are not physically present together. These results are consistent with ascorbate acting on the adrenergic receptor. Ascorbate may play a role in shock and asthma treatments, and potentiate the cardiovascular health consequences of PPA and ephedrine (Ephedra).