SUMMARY Transplantation of arteries into the anterior eye chamber rats for 8 weeks was used to test the hypothesis that the oeurohumoral enrironment is important in establishing the altered membrane potential (observable during electrogenic ion transport inhibition) of vascular muscle in hypertension. When caudal arteries from 12- to 16-week-old spontaneously hypertensive rats (SHR) or genetically matched Kyoto-Wistar normotensive rats (KNR) were transplanted into the opposite strain, there was no change in the transportinhibited membrane potential (Em) of the arterial muscle cells from that found in freshly excised donor arteries. However, when caudal arteries from 2-week-old animals were transplanted into the anterior eye chamber, the arteries always developed appropriate Emfor the host animal. In other words, a genetically KNR artery developed the Emof an SHR artery in an SHR host; conversely, a genetically SHR developed the Emof a KNR artery in the KNR host. These results provide evidence that: 1) differences between the Emof caudal arteries from SHR and KNR are not inherent in those muscle cells; 2) the change in Emis triggered in young animals preceding development of hypertension, but not after hypertension is established; and 3) the Emalteration of the caudal artery is independent structural changes that occur in artery as a result of increased blood pressure (because KNR transplants were not connected in series with the host anterior eye chamber vasculature and subject to the elevated blood pressures). We conclude that the arterial muscle cells up to a certain age respond an external factor that regulates their E$ and presumably their sensitivity to vasopressor agents.