PIO 216: Auto-regulation Of Renal Blood Flow.

Abia State University

Study guide, mechanism and notes.

The need to maintain constancy in the renal blood flow lies on the fact that the renal blood
flow has direct proportionality with the renal arterial pressure, renal venous pressure and
inversely related to the renal muscular resistance. The renal blood flow determines the
glomerular filtration rate(GFR). The large amount of blow flow and its constancy to the
kidney serves to ensure a sufficient GFR for the removal of waste products of metabolism.
This is achieved through auto-regulation.
Auto-regulation (a process not involving hormonal and nervous application) is the intrinsic
ability of an organ(kidney in this context) to regulate its own blow flow. It keeps the renal
blood flow constant, hence GFR. Two mechanisms are involved in renal auto-regulation.
(a) Myogenic response
(b)Tubulo-glomerular feedback mechanisms.
(a) Myogenic response: This deals with arterial smooth muscle constrictions and relaxation
in response to increased and decreased vessel wall pressure respectively.
(b) Tubulo-glomerular feedback mechanisms: This is a mechanism that regulates GFR which
may be altered by changes in tubular renal blood flow. It does this with cells of
juxtaglomerular apparatus which includes: macula densa( situated in the terminal portion of
ascending loop of henle(ALH). This site is where the ALH tick touches the glomerulus),
juxtaglomerular cells and the extra and intraglomerular mesangial cell( or glomerular
mesangial cell). The macula densa of the juxtaglomerular apparatus in the terminal portion
of the tick ascending segment/limb is sensitive to sodium chloride in the tubular fluid.
When the glomerular filtrate passes through the terminal portion of ALH thick, macula
densa detects the concentration of sodium chloride in the tubular fluid and accordingly alters
the glomerular blood flow, hence GFR.
When there is an increase in sodium chloride concentration in the filtrate, this means that
there is an increase in blood flow through glomerulus and a corresponding increase in GFR.
The macula densa releases adenosine from ATP. Adenosine causes constriction of afferent
arteriole thereby decreasing blood flow through glomerulus and a corresponding decrease in
GFR.
When there is a decrease in sodium chloride concentration in the filtrate, this means that
there is decrease in blood flow through the glomerulus and a corresponding decrease in
GFR. The macula densa stimulates extraglomerular mesangial cell to secrete prostaglandin
E2 which causes dilation of the afferent arteriole. It also stimulates the secretion of renin by
juxtaglomerular cells which leads to the formation of angiotensin II. Angiotensin II causes the
constriction of efferent arteriole.
The dilation of afferent arteriole and constriction of efferent arteriole leads to increase in
glomerular blood flow, hence GFR.