Angiotensin II constricts Efferent arteriole leading to increase P GC which maintains GFR. Due to Efferent arteriole constriction by Angiotensin II, renal blood flow is decreased, so flow through peritubular capillaries is decreased leading to sodium and water reabsorption. NO causes renal vasodilatation, GFR is increased. Postaglandins, Bradykinin cause increase GFR.
Strong activationof the renal sympathetic nerves can constrict the renal arterioles and decrease renal blood flow.
The renal sympathetic nerves seem to be most important in reducing GFR during severe, acute disturbances lasting for a few minutes to a few hours,such as those elicited by the defense reaction, brain ischemia, or severe hemorrhage.
diffuse thickening of the glomerular capillary wall due to the accumulation of Ig deposits along the subepithelial side of the GBM thickened GBM producing “duplication”, as if formation of a new basement Membrame above the existing 1 Membranous Nephropathy
1)subepithelial humps, as in acute glomerulonephritis 2) epimembranous deposits, as in MGN 3) subendothelial deposits, as in SLE nephritis & MPGN 4) mesangial deposits, as in IgA nephropathy 5) basement membrane. EN = endothelium EP = epithelium LD = lamina densa LRE = lamina rara externa LRI = lamina rara interna MC = mesangial cell MM = mesangial matrix