Although the RBF falls in response to AII, the fall in GFR is not of equal magnitude because AII maintains pressure within the glomerular capillary by causing greater vasoconstriction of the efferent than of the afferent arteriole.
dilating the afferent arteriole to increase renal blood flow.
constricting the afferent arteriole to increase intraglomerular pressure.
The myogenic mechanism is based on the function of baroreceptors (stretch receptors) in the afferent arterioles. When the MAP increases, these receptors respond to the increased vascular wall tension or stretch and cause afferent arteriolar constriction.
The vasodilatory prostaglandins act primarily on the afferent arterioles, counteracting the vasoconstrictive effects of angiotensin II mid SNS stimulation, and maintaining RBF despite systemic arteriolar vasoconstriction.
The walls of afferent arterioles were effaced by smudgy eosinophilic material that severely narrowed the vessel lumens, and nuclear pyknosis and karyorrhexis were seen within the altered arteriolar walls (Figure 1).
The afferent arterioles showed amorphous eosinophilic material effacing the media.
For patient 6, immunofluorescence microscopy revealed granular deposits of IgG, IgM, C1q, C3, and C4 in the glomeruli along the glomerular capillary loops and in afferent arterioles. Electron microscopy demonstrated numerous epimembranous and intramembranous electrondense deposits and small mesangial deposits.
In the kidneys, afferent arterioles involved by a lupus microangiopathy contained pyknotic nuclear material that stained prominently with the TUNEL technique.
The alveolar walls do not show the homogeneous eosinophilic alteration seen in the afferent arterioles. This is probably because the alveolar walls are thin and lack a media in which apoptosis is seen in the renal arterioles.