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Previously, we demonstrated that rats undergoing vasopressin escape bad increased mean arterial blood pressure (MAP), plasma and urine aldosterone, and increased renal protein abundance of the [alpha]-subunit of the epithelial sodium channel (ENaC), the thiazide-sensitive Na-Cl cotransporter (NCC), and the 70-kDa band of [gamma]-ENaC (Song J, Hu X, Khan O, Tian Y, Verbalis JG, and Ecelbarger CA. Am J Physiol Renal Physiol 287: F1076-F1083, 2004; Ecelbarger CA, Knepper MA, and Verbalis JG. J Am Soc Nephrol 12: 207-217, 2001). 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 were replaced to clamp these hormone levels. MAP was monitored by radiotelemetry. Rats were infused with l-deamino-[8-D-arginine]-vasopressin (dDAVP) via osmotic minipumps (5 ng/h). At day 3 of dDAVP infusion, seven rats in each group were offered a liquid diet [water load (WL)] or continued on a 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-[beta]-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, [alpha]- and [gamma]-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 [gamma]-ENaC (70 kDa). Overall, the increase in aldosterone observed in vasopressin escape is not necessary for the increased expression of NCC, [alpha]- or [gamma]-ENaC or increased MAP associated with 'escape.' SIADH; adrenalectomy; mean arterial pressure; natriuresis; hyponatremia

A study was conducted to find out whether the improvement of thick ascending limb (TAL) NaCl transport in response to long-term increases in circulating vasopressin concentration is related to increased expression levels of the apical Na-K-2Cl cotransporter in the rat TAL. Results showed that vasopressin strongly upregulates the expression of the Na-K-2Cl cotransporter of the TAL and that it is likely to play a significant role in the long-term modulation of the countercurrent multiplication system.

Long-term regulation of renal Na-dependent cotransporters and ENaC: response to altered acid-base intake. Am J Physiol Renal Physiol 279: F459-F467, 2000.--Increased systemic acid intake is associated with an increase in apical Na/H exchange in the renal proximal tubule mediated by the type 3 Na/H exchanger (NHE3). Because NHE3 mediates both proton secretion and Na absorption, increased NHE3 activity could inappropriately perturb Na balance unless there are compensatory changes in Na handling. In this study, we use semiquantitative immunoblotting of rat kidneys to investigate whether acid loading is associated with compensatory decreases in the abundance of renal tubule Na transporters other than NHE3. Long-term (i.e., 7-day) acid loading with [NH.sub.4]Cl produced large decreases in the abundances of the thiazide-sensitive Na-C1 cotransporter (TSC/NCC) of the distal convoluted tubule and both the [Beta] and [Gamma]-subunits of the amiloride-sensitive epithelial Na channel (ENaC) of the collecting duct. In addition, the renal cortical abundance of the proximal type 2 Na-dependent phosphate transporter (NaPi-2) was markedly decreased. In contrast, abundances of the bumetanide-sensitive Na-K-2C1 cotransporter of the thick ascending limb and the [Alpha]-subunit of ENaC were unchanged. A similar profile of changes was seen with short-term (16-h) acid loading. Long-term (7-day) base loading with NaH[CO.sub.3] resulted in the opposite pattern of response with marked increases in the abundances of the [Beta]- and [Gamma]-subunits of ENaC and NaPi-2. These adaptations may play critical roles in the maintenance in Na balance when changes in acid-base balance occur. sodium-proton exchange; sodium-potassium-2 chloride cotransport; distal convoluted tubule; collecting duct; amiloride-sensitive epithelial sodium channel

Na + /H + exchangers (NHE) mediate at least part of Na + entry into gill epithelia via Na + /NH 4 + exchange. For homeostasis, Na + /K + /K + /K + /K + /K + /K + ATPase. Since NHE mRNA expression does not differ, we measured the Na + -dependence of pH-induced Na + fluxes in gill vesicles from warm- and cold-acclimated fathead minnows at 20 o and 7 °C, and calculated maximum transport rates (V max K + K 1/2 s. We also measured NH 4 + -induced Na + fluxes and Na + -induced H + K max s were 278 ± 33 and 149 ± 23 arbitrary unit/s (au/s) and Na + K 1/2 s were 12 ± 4 and 6 ± 4 mmol/l when assayed at 20 o K max s were 288 ± 35 and 141 ± 13 au/s and Na + K 1/2 s 17 ± 5 and 7 ± 2 mmol/l when assayed at 20 o and 7 °C (p < 0.002), respectively. Na + -induced H + fluxes were 98 ± 8 and 104 ± 26 au/s in warm- and cold-acclimated fish assayed at 20 °C, respectively. Na + /K 4 + exchange was 120 ± 11 and 158 ± 13 au/s in warm- and cold-acclimated fish, respectively. Conclusions: Gill NHE activity was greater in warm- than cold-acclimated fish assayed at acclimation temperatures. The temperature dependence of NHE activity was similar in both groups, but differed from that reported for Na + /K + ATPase suggesting complex mechanisms to maintain Na + homeostasis., (Copyright © 2021 Elsevier Inc. All rights reserved.)