The idea that Na+ retention inevitably leads to water retention is compelling; however, were Na+ accumulation in part osmotically inactive, regulatory alternatives would be available. In rats, the relationship between total body (TB) Na+, K+, and water content is dependent on age, dietary salt intake, and mineralocorticoid activity. Growth led to mobilization of osmotically inactive Na+. This growth programmed Na+ loss originated from the bone and the completely skinned and bone-removed carcasses. Compared to high-salt, 4 weeks low-salt reduced TBNa+ by 9%. This dietary-induced Na+ loss was primarily osmotically inactive and originated from the skin. Low-salt for 1 week did not signifcantly reduce skin Na+ content. Deoxycorticosterone (DOCA) + salt treatment for 5 consecutive weeks increased TBNa+ by approximately 40%. However, water-free Na+ retention allowed the rats to maintain the ECV close to normal. Isoosmolality despite Na+ excess was achieved by two distinct mechanisms, namely osmotically inactive Na+ storage, and osmotically neutral Na+ retention balanced by K+ loss. This internal Na+ escape allowed the maintenance of volume homeostasis despite increased TBNa+. Additional ovariectomy in the DOCA-salt model reduced the osmotically inactive Na+ storage capacity, resulting in greater volume retention despite similar Na+ retention and further blood pressure increase. Extrarenal Na+ and volume balance appear to play an important role in long-term volume and MAP control.