glomerular filtration rate and renal blood flow

forces against filtration

- Hydrostatic pressure in bowman's space. This acts against letting fluid in. kidney stones can increase hydrostatic pressure in bowmans capsule - Colloid osmotic pressure in capillaries as filtration occurs, colloid osmotic pressure in the glomerular capillaries start to increase

sympathetic system

- fight or flight reaction--generally mild response. little change in GFR - cardiovascular shock--can be pronounced and even result in renal failure--GFR goes to 0 - increased sympathetic activity - leads to increased vasoconstriction - AA and EA constricts - this decreases renal plasma flow - hence GFR is decreased

myogenic mechanism

- increase in pressure stretches the blood vessels and opens stretch activated cation channels in smooth muscle cells. - The membrane depolarization opens voltage dependent calcium channels and intracellular calcium ion conc inceases, causing smooth muscle contraction. - Vessel lumen diameter decreases and vascular resistance increases - pressure is decreased to go back to normal hence no overall change in GFR

renin-angiotensin system -->role of granular juxtaglomerular cells

- juxtaglomerular cells are located in the afferent arteriole. it stores and secretes renin - renin is a proteolytic enzyme. it converts angiotensinogen II to angiotensin I - angiotensin I is converted to angiotensin II by angiotensin converting enzyme (ACE) - angiotensin II directly increases total peripheral resistance and hence systemic blood pressure - it also indirectly affects sodium reabsorption by acting on the principle cells - it increases sodium reabsorption, potassium secretion and ECF volume - If ACE is blocked, blood pressure is reduced—mechanism used in drugs to treat hypertension overall, it increases blood pressure in response to decreased blood pressure at AA

tubuloglomerular feedback mechanism

- macula densa detects flow rate and NaCl conc - increase in GFR leads to increased NaCl delivery to the macula densa - there is increased salt reabsorption at the macula densa and ATP release - ATP is metabolised into ADP, AMP and adenosine - adenosine binds to receptors in afferent arteriole and causes vasoconstriction - blood flow and GFR are returned to normal - Sensitivity of the tubuloglomerular feedback mechanism is altered by changes in local renin activity but adenosine, not angiotensin II, is the vasoconstricting agent. - Without autoregulation, increases in arterial blood pressure would lead to dramatic increases in GFR and potentially serious losses of NaCl and water from the ECF.

what are the 3 mechanisms that regulate GFR

- renin-angiotensin system - autoregulation - sympathetic system

what 2 mechanisms account of autoregulation

1) myogenic mechanism 2) tubuloglomerular feedback

regulation of GFR

depends on resistance of AA and EA. an increase in MAP by 25% would mean that GFR increases by 25% and hence there is a loss of 40L/day however there is tight regulation of GFR that takes place to prevent this. the range of autoregulation is from 80 to 200mmHg-->within this range, GFR remains constant --> this is managed by regulating vascular resistance--acts as a buffer - Flow rate is controlled so GFR is controlled in the autoregulatory range - Autoregulation is an intrinsic property of the kidneys - When the blood pressure is raised or lowered, vessels upstream of the glomerulus (afferent arterioles) constrict or dilate, thereby maintaining constant glomerular flow and capillary pressure - Below or above the autoregulatory range of pressures, blood flow and GFR change with arterial blood pressure

what is the benefit of efferent arteriole having higher colloid osmotic pressure

efferent arteriole becomes peritubular capillaries which are involved in reabsorption

definition of glomerular filtration rate

it is the volume of filtrate produced per minute - women: approx. 115ml/min - men: approx 125ml/min 180L/day entire blood filtered every 40 mins and blood volume is about 5.5L

What effect does altering the resistance of the AA and EA have on glomerular capillary pressure?

low resistance in AA and high resistance in EA gives rise to high glomerular capillary pressure • Afferent arteriole dilation, resulting from low resistance, increases glomerular blood flow and glomerular capillary pressure and therefore produces an increase in GFR • Afferent arteriole constriction produces the exact opposite effects • Efferent arteriolar dilation increases glomerular blood flow but leads to a fall in GFR because of decreased glomerular capillary pressure • Constriction of the efferent arteriole increases glomerular capillary pressure but decreases flow rate • with modest efferent arteriolar constriction, GFR increases because of the increase glomerular capillary pressure • with extreme efferent arteriolar constriction, however, GFR decreases because of the marked decrease in glomerular blood flow

what controls glomerular capillary pressure

resistance in afferent and efferent arteriole controls glomerular capillary pressure - afferent arteriole is wider than the efferent arteriole the resistances of the AA and EA are controlled by neural and hormonal inputs. can also be controlled intrinsically

why is it important to maintain the glomerular capillary pressure at constant

this ensures that glomerular filtration rate is constant

what 2 things does glomerular filtration depend on

ultrafiltration coefficient net starlings forces (refer to equation)

glomerular filtration pressure balance

• There is a balance of hydrostatic and colloid osmotic pressures • Forces act across the glomerular filtration membrane • Hydrostatic pressure depends on the arterial blood pressure and the resistances of upstream and downstream blood vessels • Colloid osmotic pressure in bowmans space is due to proteins (0.1% of proteins get filtrated which gives rise to this pressure). Oncotic pressure here is also in favour of filtration but this pressure is too small so not very significant in a healthy person (refer to slide 7-11)