Ans. is 'c' i.e., Tubulo-glomerular feedback Autoregulation of GFRThe GFR is normally well autoregulated in the range of 70-180 mm Hg of systemic pressure. Feedback mechanisms intrinsic to the kidney normally keep the renal blood flow and GFR relatively constant, despite marked changes in aerial blood pressure. The relative constancy of GFR and renal blood flow is referred to as autoregulation. The primary function of autoregulation in other tissues (other than kidneys) is to maintain the delivery of oxygen and nutrient at a normal level and to remove the waste products of metabolism, despite changes in aerial pressure. In the kidneys, the non-nal blood flow is much higher than that required for these functions. the major function of autoregulation in the kidney is to maintain a relatively constant GFR and to allow precise control of renal excretion of water and solutes.There are two plausible hypotheses for explaining the autoregulation of GFR (i) Tubuloglomerular feedback hypothesis, and (ii) Myogenic hypothesis.Tubulo-glomerular feedbackTo perform the function of autoregulation, the kidneys have a feedback mechanism that links changes in sodium chloride concentration at the macula densa with the control of renal aeriolar resistance. This feedback helps to ensure a relative constant delivery of sodium chloride to the distal tubule and helps prevent spurious fluctuations in renal excretion that would otherwise occur.The tubuloglomerular feedback mechanism has two components that act together to control GFR : - i) An afferent aeriolar feedback mechanism (usually this component is referred to as tubuloglomerular feedback, and ii) An efferent aeriolar feedback mechanism. These feedback mechanisms depend on the juxtaglomerular apparatus which consists of : (i) Macula densa, i.e., specialized epithelium of distal tubule where it comes in contact with afferent aeriole, (ii) Juxtaglomerular cells, i.e., modified smooth muscle cells of afferent aeriole, and iii) Lacis cells.Afferent aeriolar feedback mechanism : - Decrease in renal aeriolar pressure causes decrease in GFR and as a result low NaCI is delivered to distal tubules. This is sensed by macula densa and the signal is transmitted to afferent aerioles which causes decreased resistance of afferent aerioles. Decreased afferent aeriolar resistance increases glomerular hydrostatic pressure and therefore GFR. The transmitter involves is adenosine which causes opening of Ca*2 channels.Efferent aeriolar feedback mechanism : - Decreases GFR causes delivery of less NaCl to distal tubule, which is sensed by macula densa cells and the signal is transmitted to juxtaglomerular (JG) cells which secrete renin. As a result renin angiotensin system is activated and there is generation of angiotensin II which causes constriction of efferent aeriole. This results in increased glomerular capillary hydrostatic pressure and increased GFR.Opposite occurs when there is increase aerial pressure and increased GFR. Increased NaCl is delivered to the macula densa which causes constriction of afferent aeriole and decrease,: renin by JG cells with decreased efferent aeriole resistance.It would be wise to know about glomerulotubular balance, which may be confused by tubuloglomerular feedback.Glomerulotubular balance : - Tubular reabsorption in proximal tubules is load-dependent, i.e., when the GFR increase, the reabsorption of the filtrate in the proximal tubule increases propoionately. It occurs because tubular reabsorption is flow-limited. Because of glomerulotubular balance, the urinary Na+ output does not increase massively when the GFR increases.Myogenic AutoregulationAfferent aerioles constrict in response to augmented blood pressure. Aeriolar constriction restores GFR to normal levels. Possibly, stretching of aerioles leads to the opening of stretch - sensitive Ca+2 channels on aeriolar smooth muscle cells resulting in a Ca+ influx that causes the cells to contract.