A principal, and unique, renal effector site for angiotensin II (ANG II) is the efferent arteriole, and that has generated considerable interest regarding potential benefits of ANG II inhibition in the treatment and prevention of diabetic renal injury. A hallmark complication of long-standing diabetes is glomerular injury, and there is substantial evidence that lowering glomerular hydrostatic pressure attenuates the injury process. One way that has been accomplished is by lowering arterial pressure, but additional evidence suggests that anti-hypertensive treatment with ANG II inhibition provides even greater protection because of the associated efferent arteriolar dilation. Because of that action, ANG II inhibition in diabetes has been advocated even without diagnosis of hypertension, and the benefits of that treatment have been ascribed largely to the effect of decreased efferent arteriolar resistance to lower glomerular hydrostatic pressure. However, that renal vascular action of ANG II, together with powerful direct effects on tubular sodium reabsorption, underlie its dominant influence on chronic arterial pressure control. Moreover, the influence of ANG II on arterial pressure is not limited to hypertension; it contributes significantly to the maintenance of blood pressure when plasma ANG II levels are normal or even reduced. Thus, while acknowledging that efferent arteriolar dilation is a unique intrarenal benefit associated with ANG II inhibition, this review will focus on how and why inhibition of the multiple intrarenal actions of ANG II also protect the kidneys through systemic mechanisms, even when blood pressure and ANG II are not increased.
- Angiotensin II
- Arterial pressure
- Sodium excretion
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism