BACKGROUND: In vitro studies have demonstrated that aldosterone elicits nongenomic actions by enhancing protein expressions of phosphorylated epidermal growth factor receptor (pEGFR) and phosphorylated extracellular signal-regulated kinases 1/2 (pERK1/2). There are no available in vivo investigations regarding this action of aldosterone on renal pEGFR-pERK1/2 protein expressions. METHODS: Male Wistar rats received normal saline solution, low-dose (LA: 150 μg/kg BW) or high-dose aldosterone (HA: 500 μg/kg BW) by intraperitoneal injection. After 30 min, protein abundances and localizations of renal pEGFR and pERK1/2 were determined by Western blot and immunohistochemistry. RESULTS: Plasma aldosterone levels were increased in LA and HA groups (p < 0.001). Aldosterone enhanced renal pEGFR and pERK1/2 protein abundances (p < 0.001). HA showed a greater stimulation on pEGFR immunoreactivity than LA in the glomerulus, vasa recta, and thin limb of Henle's loop in the inner medulla area. LA provided more reactivity of pERK1/2 in the thick ascending limb of Henle's loop, outer medullary collecting duct, and proximal straight tubule, whereas HA illustrated more pERK1/2 activation in the glomerulus, peritubular capillary, and inner medulla region. CONCLUSION: This is the first in vivo study which demonstrates that aldosterone, via the nongenomic pathway, could elevate pEGFR and pERK1/2 protein abundances and expressions in the rat kidney. These results indicate that aldosterone induces phosphorylation of EGFR upstream of ERK1/2.
BACKGROUND: In vitro studies have demonstrated that aldosterone elicits nongenomic actions by enhancing protein expressions of phosphorylated epidermal growth factor receptor (pEGFR) and phosphorylated extracellular signal-regulated kinases 1/2 (pERK1/2). There are no available in vivo investigations regarding this action of aldosterone on renal pEGFR-pERK1/2 protein expressions. METHODS: Male Wistar rats received normal saline solution, low-dose (LA: 150 μg/kg BW) or high-dose aldosterone (HA: 500 μg/kg BW) by intraperitoneal injection. After 30 min, protein abundances and localizations of renal pEGFR and pERK1/2 were determined by Western blot and immunohistochemistry. RESULTS: Plasma aldosterone levels were increased in LA and HA groups (p < 0.001). Aldosterone enhanced renal pEGFR and pERK1/2 protein abundances (p < 0.001). HA showed a greater stimulation on pEGFR immunoreactivity than LA in the glomerulus, vasa recta, and thin limb of Henle's loop in the inner medulla area. LA provided more reactivity of pERK1/2 in the thick ascending limb of Henle's loop, outer medullary collecting duct, and proximal straight tubule, whereas HA illustrated more pERK1/2 activation in the glomerulus, peritubular capillary, and inner medulla region. CONCLUSION: This is the first in vivo study which demonstrates that aldosterone, via the nongenomic pathway, could elevate pEGFR and pERK1/2 protein abundances and expressions in the rat kidney. These results indicate that aldosterone induces phosphorylation of EGFR upstream of ERK1/2.