Figure 142

Vasoactive hormones that may be responsible for the hemodynamic abnormalities in acute tubule necrosis (ATN). A persistent reduction in renal blood flow has been demonstrated in both animal models of acute renal failure (ARF) and in humans with ATN. The mechanisms responsible for the hemodynamic alterations in ARF involve an increase in the intrarenal activity of vasoconstrictors and a deficiency of important vasodilators. A number of vasoconstrictors have been implicated in the reduction in renal blood flow in ARF. The importance of individual vasoconstrictor hormones in ARF probably varies to some extent with the cause of the renal injury. A deficiency of vasodilators such as endothelium-derived nitric oxide (EDNO) and/or prostaglandin I2 (PGI2) also contributes to the renal hypoperfusion associated with ARF. This imbalance in intrarenal vasoactive hormones favoring vasoconstriction causes persistent intrarenal hypoxia, thereby exacerbating tubular injury and protracting the course of ARF.

Glomerular basement membrane

Glomerular capillary endothelial cells

Glomerular epithelial cells

Mesangial cell contraction Angiotensin II Endothelin-1 Thromboxane Sympathetic nerves

Mesangial cell contraction Angiotensin II Endothelin-1 Thromboxane Sympathetic nerves

Glomerular basement membrane

Glomerular capillary endothelial cells

Glomerular epithelial cells

Mesangial cell relaxation Prostacyclin EDNO

0 0

Post a comment