Regulation Of Gfr

REGULATION OF GFR

Q. 1

The tubuloglomerular feedback is mediated by:

 A

Sensing of Na+ concentration in the macula densa

 B

Sensing of C1+ concentration in macula densa

 C

Sensing NaCl concentration in the macula densa

 D

Opening up of voltage gated Na+ channels in afferent arteriole

Q. 1

The tubuloglomerular feedback is mediated by:

 A

Sensing of Na+ concentration in the macula densa

 B

Sensing of C1+ concentration in macula densa

 C

Sensing NaCl concentration in the macula densa

 D

Opening up of voltage gated Na+ channels in afferent arteriole

Ans. C

Explanation:

In the tubuloglomerular feedback mechanism, ATP and adenosine form a cascade of signaling molecules that adjust vascular tone to the salt concentration at the macula densa.

Ref: Reviews of Physiology, Biochemistry and Pharmacology By Frank Schweda, Volume 161, 2011, Page 21.

Q. 2

All of the following statements about angiotensin II are TRUE, EXCEPT:

 A

Autoregulation of GFR

 B

Release aldosrerone

 C

Secreted from endothelium

 D

Constriction of afferent arteriole

Q. 2

All of the following statements about angiotensin II are TRUE, EXCEPT:

 A

Autoregulation of GFR

 B

Release aldosrerone

 C

Secreted from endothelium

 D

Constriction of afferent arteriole

Ans. C

Explanation:

Angiotensinogen is the circulating protein substrate from which renin cleaves angiotensin I. It is synthesized in the liver within a few seconds to minutes after formation of angiotensin I, two additional amino acid are split from the angiotensin I to from the 8-amino acid peptide angiotensin II. This conversation occurs almost entirely in the lungs while the blood flows through the small vessels of lungs, catalyzed by an enzyme called angiotensin converting enzyme (ACE) that is present in the endothelium of the lungs vessels. 

 
FUNCTION:
Angiotensin II is an extremely powerful vasoconstrictor. Vasoconstrictor occurs intensely in the arterioles and much less so in the veins. It decrease excretion of both slowly salt and water by the kidneys. This slowly increases the extracellular fluid volume, which then increase the arterial pressure during subsequent hours and days. It exerts important actions at vascular smooth muscle, adrenal cortex, kidney, heart and brain.
 
Act directly on the zona glomerulosa of the adrenal cortex to stimulate aldosterone biosynthesis. At higher concentrations, angiotensin II also stimulates glucocorticoid biosynthesis. Angiotensin II act on the kidney to cause renal vasoconstriction, contraction of mesangial cells with a resultant decrease in GFR increase proximal tubular sodium reabsorption, and inhibit the secretion of renin. In addition to its central effects on blood pressure, angiotensin II acts on the central nervous system to stimulate drinking (dipsogenic effect ) and increase the secretion of vasopressin and adrenocorticotropic hormone (ACTH).
 
Ref: Ganong 23/e, page 670 ; Guyton 11/e, page 201-02,223-24,907

Q. 3

According to myogenic hypothesis of renal autoregulation, the afferent arterioles contract in response to stretch induced by:

 A

No release

 B

Narodrenaline release

 C

Opening of Ca2+ channels

 D

Adenosine release

Q. 3

According to myogenic hypothesis of renal autoregulation, the afferent arterioles contract in response to stretch induced by:

 A

No release

 B

Narodrenaline release

 C

Opening of Ca2+ channels

 D

Adenosine release

Ans. C

Explanation:

C i.e. Opening of Ca2+ channels


Q. 4

The tubuloglomerular feedback is mediated by:

 A

Sensing of Na+ concentration in the macula densa

 B

Sensing of Cl+ concentration in macula densa

 C

Sensing NaCl concentration in the macula densa

 D

Opening up of voltage gated Na+ channels in afferent arteriole

Q. 4

The tubuloglomerular feedback is mediated by:

 A

Sensing of Na+ concentration in the macula densa

 B

Sensing of Cl+ concentration in macula densa

 C

Sensing NaCl concentration in the macula densa

 D

Opening up of voltage gated Na+ channels in afferent arteriole

Ans. C

Explanation:

C i.e. Sensing NaC1 concentration in the macula densa

‘To perform the function of auto regulation, the kidneys have a feed back mechanism (tubuloglomerular feed back) that links changes in sodium chloride concentration at the macula densa (tubular component) with the control of renal arteriolar resistance. (glomerular component).


Q. 5

With increased flow to loop of Henle, decreased in GFR is by ‑

 A

Countercurrent exchanger

 B

Glomerulotubular balance

 C

Tubulo-glomerular feedback

 D

Countercurrent multiplier

Q. 5

With increased flow to loop of Henle, decreased in GFR is by ‑

 A

Countercurrent exchanger

 B

Glomerulotubular balance

 C

Tubulo-glomerular feedback

 D

Countercurrent multiplier

Ans. C

Explanation:

Ans. is ‘c’ i.e., Tubulo-glomerular feedback

Autoregulation of GFR

  • The 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 arterial 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 arterial 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 feedback

  • To 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 arteriolar 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 arteriolar feedback mechanism (usually this component is referred to as tubuloglomerular feedback, and ii) An efferent arteriolar 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 arteriole, (ii) Juxtaglomerular cells, i.e., modified smooth muscle cells of afferent arteriole, and iii) Lacis cells.
  1. Afferent arteriolar feedback mechanism : – Decrease in renal arteriolar 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 arterioles which causes decreased resistance of afferent arterioles. Decreased afferent arteriolar resistance increases glomerular hydrostatic pressure and therefore GFR. The transmitter involves is adenosine which causes opening of Ca*2 channels.
  2. Efferent arteriolar 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 arteriole. This results in increased glomerular capillary hydrostatic pressure and increased GFR.
  • Opposite occurs when there is increase arterial pressure and increased GFR. Increased NaCl is delivered to the macula densa which causes constriction of afferent arteriole and decrease,: renin by JG cells with decreased efferent arteriole 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 proportionately. 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 Autoregulation

  • Afferent arterioles constrict in response to augmented blood pressure. Arteriolar constriction restores GFR to normal levels. Possibly, stretching of arterioles leads to the opening of stretch – sensitive Ca+2 channels on arteriolar smooth muscle cells resulting in a Ca+ influx that causes the cells to contract.


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