Aldosterone Rapidly Enhances Levels of the Striatin and Caveolin-1 Proteins in Rat Kidney: The Role of the Mineralocorticoid Receptor

BACKGROUND: Striatin and caveolin-1 (cav-1) are scaffolding/regulating proteins that are associated with salt-sensitive high blood pressure and promote renal sodium and water reabsorption, respectively. The mineralocorticoid receptor (MR) interacts with striatin and cav-1, while aldosterone increases striatin and cav-1 levels. However, no in vivo data have been reported for the levels of these proteins in the kidney. METHODS: Male Wistar rats were intraperitoneally injected with normal saline solution, aldosterone alone (Aldo: 150 µg/kg body weight), or aldosterone after pretreatment with eplerenone, an MR blocker, 30 minutes before the aldosterone injection (eplerenone [Ep.]+Aldo). Thirty minutes after the aldosterone injection, the amount and localization of striatin and cav-1 were determined by Western blot analysis and immunohistochemistry, respectively. RESULTS: Aldosterone increased striatin levels by 150% (P<0.05), and cav-1 levels by 200% (P<0.001). Eplerenone had no significant effect on striatin levels, but partially blocked the aldosterone-induced increase in cav-1 levels. Aldosterone stimulated striatin and cav-1 immunoreactivity in both the cortex and medulla. Eplerenone reduced cav-1 immunostaining in both areas; however, striatin intensity was reduced in the cortex, but increased in the medulla. CONCLUSION: This is the first in vivo study demonstrating that aldosterone rapidly enhances renal levels of striatin and cav-1. Aldosterone increases striatin levels via an MR-independent pathway, whereas cav-1 is partially regulated through MR.

Effects of vanadate and potassium depletion on renal H, K-ATPase protein expression

Background: Vanadate (V) inhibits while potassium (K) depletion stimulates collecting tubule H, K-ATPase activity. In the presence of V, K depletion could not restore the decreased H,K-ATPase activity. The effects of V and K depletion on renal H,K-ATPase protein expression might explain such observation.Objective: To examine the effects of V and K depletion on renal H,K-ATPase protein expression. Methods: Rats treated with normal saline solution (NSS) or V (5 mg/kg body weight) received either normal potassium (NK) or low potassium (LK) diet for 10 days. Protein expressions of renal H,K-ATPase \α₁ and \α₂ isoforms were determined by immunohistochemistry.Results: Both NK and LK animals treated with V had significantly increased vanadium levels in serum, urine, and renal tissues. LK diet caused hypokalemia. Animals treated with LK and V showed progressive hypokalemia. LK stimulated renal H,K-ATPase \α₁ protein expression in both cortex and medulla but enhanced H,K-ATPase \α₂ protein expression only in the cortex. Vanadate did not affect H,K-ATPase \α₁ protein expression in both NK and LK groups. Vanadate unaltered H,K-ATPase \α₂ protein expression in NK animals but could attenuate the increased expression in LK group.Conclusion: The magnitude of direct inhibitory effect of V on renal H,K-ATPase activity with small suppressive effect on protein expression is greater than the stimulatory effect of K depletion on H,K-ATPase activity and protein expression.