Role of tubuloglomerular feedback in autoregulation of GFR
The tubuloglomerular feedback mechanism has two components that act together to control GFR: an afferent arteriolar feedback mechanism an efferent arteriolar feedback mechanism. These feedback mechanisms depend on special anatomical arrangements of the juxtaglomerular complex.The juxtaglomerular complex consists of: macula densa cells in the initial portion of the distal tubule. juxtaglomerular cells in the walls of the afferent and efferent arterioles. The macula densa is a specialized group of epithelial cells in the distal tubules that comes in close contact with the afferent and efferent arterioles.
Constrictor action of angiotensin II on efferent arterioles helps prevent serious reductions in glomerular H P and GFR when renal perfusion pressure falls below normal. The administration of drugs that block the formation of angiotensin II(angiotensin-converting enzyme inhibitors) or that block the action of angiotensinII (angiotensin II antagonists) causes greater reductions in GFR than usual when the renal arterial pressure falls below normal.
Myogenic autoregulation
Its the ability of individual blood vessels to resist stretching during increased arterial pressure to maintain renal blood flow and GFR relatively constant. Mechanism :increased wall tension (wall stretch) by contraction of the vascular smooth muscle. This stretch allows increased movement of calcium ions from the ECF into the cells, causing them to contract this contraction prevents over distention of the vessel & raising vascular resistance, helps prevent excessive increases in renal blood flow and GFR when arterial pressure increases.High protein intake and increased blood glucoseA high protein intake (large amounts of meat) ↑↑ both renal blood flow and GFR. due to growth of the kidneys. Mechanism :A high-protein meal ↑↑ the release of amino acids into the blood &reabsorbed in the proximal tubule. This stimulates sodium reabsorption from proximal tubule & decreases sodium delivery to the macula densa (and by a tubuloglomerular feedback)–mediated decrease in resistance of the afferent arterioles which then raises renal blood flow and GFR.
A similar mechanism may also explain the marked increases in renal blood flow and GFR that occur with large increases in blood glucose levels in uncontrolled diabetes mellitus.
An opposite sequence of events occurs when proximal tubular reabsorption is reduced. ( e g: when the proximal tubules are damaged (poisoning by heavy metals, mercury, large doses of tetracyclines) their ability to reabsorb Nacl is ↓↓. So large amounts of Nacl are delivered to the distal tubule and, without good compensations, this cause excessive volume depletion.