Previously we demonstrated that rats undergoing vasopressin-escape had increased mean arterial blood pressure (MAP), plasma and urine aldosterone and increased renal protein abundance of the -subunit of the epithelial sodium channel (ENaC), the thiazide-sensitive Na-Cl cotransporter (NCC), and the 70-kDa band of -ENaC. Here we determine whether changes in these renal proteins and MAP require elevated aldosterone levels. We performed adrenalectomies (ADX) or sham surgeries on male, Sprague-Dawley rats. Corticosterone and aldosterone was replaced to clamp these hormone levels. MAP was monitored by radiotelemetry. Rats were infused with 1-deamino-[8-D-arginine]-vasopressin (dDAVP) via osmotic minipumps (5 ng/hr). At day 3 of dDAVP infusion, 7 rats in each group were offered liquid diet (water-load, WL) or continued on solid diet (SD). Plasma aldosterone and corticosterone and urine aldosterone were increased by WL in sham rats. ADX-WL rats escaped, as assessed by early natriuresis followed by diuresis, however, urine volume and natriuresis were somewhat blunted. WL did not reduce the abundance or activity of 11--hydroxsteroid dehydrogenase type 2. Furthermore, the previously observed increase in renal aldosterone-sensitive proteins and escape-associated increased MAP persisted in clamped rats. The densitometry of immunoblots for NCC, - and -70 kDa ENaC, respectively were (% sham-SD): sham-WL, 159, 278, 233; ADX-SD, 69, 212, 171; ADX-WL, 116, 302, 161. However, clamping corticosteroids blunted the rise at least for NCC and -ENaC (70 kDa). Overall, the increase in aldosterone observed in vasopressin-escape is not necessary for the increased expression of NCC, - or -ENaC or increased MAP associated with "escape".