Aldosterone-dependent NCC activation

Aldosterone acutely stimulates NCC activity via a SPAK-mediated pathway.

Hypertension is a leading cause of morbidity and mortality worldwide, and disordered sodium balance has long been implicated in its pathogenesis. Aldosterone is perhaps the key regulator of sodium balance and thus blood pressure. The sodium chloride cotransporter (NCC) in the distal convoluted tubule of the kidney is a major site of sodium reabsorption and plays a key role in blood pressure reg...

Regulation of NHE3, NKCC2, and NCC abundance in kidney during aldosterone escape phenomenon: role of NO.

Escape from aldosterone-induced renal NaCl retention is an important homeostatic mechanism in pathophysiological states in which plasma aldosterone levels are inappropriately elevated, e.g., in primary aldosteronism. Our previous studies demonstrated that the escape process occurs largely as a result of a marked suppression of the abundance of the thiazide-sensitive Na-Cl cotransporter (NCC) of...

Renin-angiotensin-aldosterone activation in heart failure, aldosterone escape.

Effect of ATP-Dependent K+ Channel Openers and Blockers on Serum Concentration of Aldosterone in Rats

There are many reports for involvement of ATP-sensitive potassium channels in pancreatic, cardiac and vascular smooth muscle cells. This study examined the effect of single doses of K+ channel openers diazoxide, minoxidil and K+ channel blockers chlorpropamide, glibenclamide on serum concentration of aldosterone in male rats. Blood samples were obtained 60 minutes after drug treatment and serum...

Regulated endocytosis of NCC.

THE THIAZIDE-SENSITIVE Na -Cl cotransporter (NCC) in the aldosterone-sensitive distal convoluted tubule (DCT) is responsible for the reabsorption of as much as 10% of filtered Na -Cl (13). Notably, this may be a significant overestimate of the quantitative contribution of NCC to renal Na -Cl handling, in light of the recent demonstration that combined activity of the apical Na -dependent Cl -HC...