How is the control of renal blood flow and glomerular filtration?

Continuing the basics of renal physiology let's talk a little about the physiological control of renal blood flow and glomerular filtration.

It is known that the high blood flow to the kidneys exceeds the metabolic demands of the tissue. The purpose of this additional flow, is to provide sufficient plasma for the high glomerular filtration rate required for precise regulation of body fluid volume and concentration of solutes.

As one might expect, the mechanisms that regulate renal blood flow are closely linked to the control of glomerular filtration and excretory functions of the kidneys.

Regulation of Renal Blood Flow

The RBF is directly proportional to the pressure gradient between the renal arteries and veins, and is inversely proportional to the resistance of the renal vessels. In addition, the resistance is caused by arterioles, because the rim has two sets of arterioles, constituting the main mechanism to vary the blood flow.

The RBF is self-regulating within the wide range of mean arterial pressure. The renal artery pressure may range from 80-200mmHg. But blood flow remains constant, because the extent to which blood pressure rises or lowers, renal resistance has to increase or decrease proportionally.

Mechanisms to control the flow and renal glomerular filtration

There are two hypotheses for the mechanism of this control:

The myogenic hypothesis, where with increased blood pressure there would be a distension of the blood vessels and therefore subsequently a reflex contraction of the smooth muscle in the vessel wall (mainly in afferent) and so this would help prevent excessive increases renal blood flow and glomerular filtration.


Other hypothesis would through tubuloglomerular feedback which is controlled by the juxtaglomerular complex. An example of this mechanism can be exemplified in the fall of blood pressure. When this occurs, automatically glomerular hydrostatic pressure drops and thus also the glomerular filtration. This causes a decrease in the amount of sodium chloride that passes through the macula densa (structure located between the proximal and distal convoluted tubules) and that causes her to secrete renin. The increased renin concentration, increases the angiotensin II, which will cause an increase in resistance of the efferent arterioles and therefore increase glomerular hydrostatic pressure and thus regulating the glomerular filtration.

The sympathetic nervous system through the alpha-1 receptors also cause vasoconstriction of the afferent and efferent arterioles thus contributing to the reduction in renal blood flow and thus the reduction of glomerular filtration.

Prostaglandins are substances involved in vasodilation. They contribute significantly because they are the modulating vasoconstrictor produced by the sympathetic nervous system and angiotensin II.

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