1. There is high pressure in the small renal arterioles ,afferent arterioles & glomerulus (100 to 80 mm.Hg.) to assist filtration of plasma at the glomerulus into the BC.
2.There is low pressures in the EA, peritubular capillaries, venioles& vasa recta(13,10,8,6mm.Hg.) to assist reabsorption of the fluid from the interstitium & tubules into them.
3.The peritubular capillaries & vasa recta absorb 4 times as much as fluid as any other capillary system in the body(180 liter filtered daily through the glomerulus only 1.5 liter becomes urine, due to:
1. 1. The low pressure .
2. 2.High porosity .
3 3.The slow flow of blood through these capillaries as only 1 to 2% of RBF pass through vasa recta.
A . Capillary endothelium with fenestra which allow passage of only small molecules.
B. Basement membrane composed of negative charged proteoglycan which impedes the passage of important negative charged plasma proteins from blood through the glomerular membrane into the urine by charge repulsion.
C. BC epithelial cells containing foot processes which oppose each other to form slit pores which allow only passage of small molecules only.
These 3 important characters of glomerular membrane prevent passage of high molecular weight(MW) proteins as albumen & allows only low MW small proteins.
Glomerular permeability(GP) = concentration at filtered side/concen. At plasma side
For example GP of Inulin (MW of 5200) is 1.
GP of very small proteins(MW of 30000) is 0.5 .
While GP of albumin(MW of 69000) is 0.005 i.e only small amounts of large MW proteins are filtered through the glomerulus.
The size of slit pores determine the passage of molecules as the pores diameter is about 80 angstromes.
The characters of glomerular membrane augment each other as although the albumin diameter is 60 angstromes but their repulsion by negative charged basement membrane proteins as they are also negatively charged prevent their passage through the glomerulus, so both characters augment each other.
So the glomerular filtrate is the same as plasma with the exception that it contains no significant amount of plasma proteins, the concentration of non protein negative charged ions as Cl & HCO3 is 5% Lower than in plasma & concentration of non protein positive ions as Na+ is 5% higher than in the plasma.
EA constriction is important& beneficial in some diseases as cirrhosis, nephrotic syndrome & congestive heart failure in which the renal blood flow & intraglomerular pressure is maintained critically by EA constriction through the effect of prostaglandins(PGs) ,so the use of PG Inhibitrss as NSAIDs ( brufen , diclofenac, etc) in these diseases may precipitate renal failure.
On the contrary EA Constriction may be harmful in other conditions as in diabetic nephropathy as the renal damage is accelerated by high intraglomerular pressure through EA constriction ,so the use of & PG inhibitors or ACEI as captopril may reduce the EA constriction ,reduce IGP & slow or reverse the renal damage in diabetic nephropathy.
GFR & RBF remain constant in the BP range of 75-160 mm.Hg, maintained by 4 factors :
1.Tubuloglomerular feedback: controlled by juxtaglomerular apparatus consisting of distal tubular cells called macula densa & AA/EF cells called juxtaglomerular cells ,so when BP is lowered causing lowering of RBF,glomerular hydrostatic pressure & GFR ,this will cause decrease Nacl delivery to the distal tubular cells (macula densa) ,this will stimulate the juxtaglomerular cells of the AA & EA to release Renin which cause release of Angiotensin1 from the liver which in turn is converted to Angiotensin 2(A2) by the enzyme Angiotensin converting enzyme secreted by the lungs & A2 is a strong vasoconstrictor causing renal arteriolar vasocosntriction specially EA vasoconstriction so maintaining glomerular hydrostatic pressure & GFR back to normal.
2.Glomerulo tubular balance & pressure diuresis by which the GFR is returned to normal when BP & RBF is increased, by increasing renal Na & water excretion (pressure diuresis) & by decreasing tubular reabsotption & vice versa.
3.Myogenic autoregulation of RBF & GFR:
When the renal arteries contract in response to increase BP to protect the renal blood flow from excess rise & vice versa dilates in reponse to low BP.
4.High protein intake & high blood glucose : which both decrease the Na delivery to the distal tubules by increasing proximal tubule Na reabsorption, as both AA & glucose are cotransported with Na in the proximal tubules, so increase AA & glucose delivery to the proximal tubules causes increasesd reabsorption of Na & decreased delivery of Na to macula densa, so activate the juxtaglomerular apparatus mentioned above, leading to increase RBF & GFR.