Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1-7) administration in anesthetized rats

摘要

the renin angiotensin system (RAS) is a powerful endogenous hormonal cascade that plays a central role in the regulation of blood pressure, sodium balance, and body fluid homeostasis. Classically, this cascade culminates in the formation of the potent vasoconstrictor, antinatriuretic and antidiuretic peptide angiotensin II (ANG II) (7, 20). ANG II is produced from angiotensin I (ANG I) primarily via angiotensin-converting enzyme (ACE) but also via the tissue enzyme chymase. The latter has been shown to contribute to the production of ANG II in the diabetic mouse kidney (21). More recently, another RAS peptide called angiotensin (1-7) [ANG (1-7)] has been described as the endogenous counter regulator of ANG II (16) via activation of its "mas" receptor (24). ANG (1-7) is formed directly from ANG II by the ACE isoform ACE 2 (27, 32) but can also be synthesized directly from ANG I via tissue-specific peptidases such as neprilysin in the kidney (2). The intrarenal actions of ANG (1-7) and its interaction with ANG II on renal hemodynamics and tubular fluid reabsorption have not been fully elucidated. Previous in vitro studies have demonstrated that exposure of isolated rat renal arteries (31) and rabbit afferent arterioles (23) to ANG (1-7) caused an increase in their diameter and that was taken as evidence for a local vasodilator action. However, the vasodilation was only demonstrated in vessels that had been preconstricted with either ANG II (31) or norepinephrine (23), suggesting that this action of ANG (1-7) was reactive as opposed to being active.