Acid–base regulation of angiotensin receptors in the kidney

Abstract

Purpose of review 

Angiotensin II (Ang II) is a major systemic regulator of blood pressure, blood volume, and acid–base homeostasis. However, the effects of local Ang II signaling in the kidney are less well known. Here we review the impact of Ang II on acid–base transport in specific nephron segments and discuss the recently described role of acid loading in sensitizing the proximal tubule to Ang II.

Recent findings 

Recent studies suggest that Ang II signaling is necessary for a normal kidney response to acid loads. Under acidic conditions, tubule cells upregulate type 1 Ang II receptors, amplifying the effects of Ang II. Site of action may also affect Ang II activity, as Ang II can produce divergent effects when acting on the luminal versus basolateral aspects of tubule cells. High luminal concentrations of Ang II and its precursors may facilitate coordinated acid–base transport and metabolic activity throughout the nephron.

Summary 

Local Ang II signaling in the kidney directly modulates acid–base transport and metabolism, providing an additional mechanism by which the renin–angiotensin–aldosterone system regulates acid–base balance. The segment-specific and acid-stimulated responses of the tubule to Ang II are diverse and merit further exploration for their adaptive and potentially maladaptive roles.