The extent of preservation of endothelial, neurogenic and vascular function following frozen storage was studied using the rabbit central ear artery and a resistance artery branch. Fresh and frozen-stored artery segments were placed in tissue baths containing a physiological buffer solution and attached to a wire myograph apparatus for measurement of isometric force. Responses to cumulative additions of norepinephrine, histamine, acetylcholine and sodium nitroprusside were compared between fresh arteries and adjacent segments that had been stored frozen for 2–8 days at –70 °C. Responses to transmural nerve stimulation were measured in central ear artery segments that were fresh or stored frozen for 13–26 days. Large and small artery segments were frozen in ampules containing newborn calf serum and 1.8 Mdimethylsulfoxide used as a cryoprotective agent. Following frozen storage, the vascular sensitivity of large and resistance arteries to norepinephrine and histamine were unaltered although maximal contractile responses were significantly reduced. Agonist affinity (K<sub>A</sub> values) to norepinephrine was also unchanged following frozen storage of large artery segments. Constrictor responses to varied frequencies of transmural nerve stimulation were similar between fresh and frozen-stored large arteries, suggesting that adrenergic nerve function is well preserved. In resistance arteries, vascular sensitivity and maximal relaxation to acetylcholine and sodium nitroprusside were unchanged. Similarly, relaxation of large arteries to sodium nitroprusside was well preserved. Although vascular sensitivity to acetylcholine was reduced in large arteries following frozen storage, much of the endothelial function was still preserved as indicated by only a 10% decrease in maximal relaxation. These results indicate that frozen storage of large and small artery segments preserves endothelial and vascular smooth muscle function as well as adrenergic neurotransmission.