On previous posts we talked about some of the mechanisms used by our bodies to maintain vascular pressure inside the normal parameters.

This time we will touch another mechanism for the control of blood pressure, in fact this is the main system for control of blood pressure in the long term, this system is the renin-angiotensis-aldosterone system also now as RAAS.

How does Renin-Angiotensin-Aldosterone System work?

There are three hormones that take part in the RAAS.

Renin.

Angiotensin.

Aldosterone.

The end result of activation of the RAAS is an increase in blood pressure through many mechanisms.

The stimuli for the activation of the system are:

Decrease in arterial mean pressure.

Decrease in the concentration of NaCl.

Decrease in blood volume.

Activation of sympathetic nervous system.

All this stimuli produce a decrease in the renal perfusion volume, this is sensed by special receptors in the kidney and the kidney starts transforming pro-renin into renin.

The renin will diffuse to the circulation where it will act upon angiotensinogen, transforming it into Angiotensin I.

In tissues like lungs, suprarrenal, endothelial smooth muscle, myocardium we will find a the converting enzyme that will act upon Angiotensin I transforming it into Angiotensin II.

Angiotensin II is an active hormone with many effects:

Contraction of the afferent and efferent arterioles in the kidney glomeruli (its effect upon the afferent arteriole is greater, this produces an increase in the GFR).

Increase in the release of aldosterone from the suprarrenal gland.

Decrease in the synthesis of renin (a negative feedback mechanism).

Increase in the activity of the Na/K pump in cells of the renal tubules (leading to an increase in the reabsorption of Na).

Increase in the activity of the cotransporter Na/HCO3 in cells of the renal tubules (leading to an increase in the reabsorption of Na).

Increase in the activity of the antiport transporter Na/H+ in intercalated cells of the renal tubules (leading to an increase in the reabsorption of Na).

Increase in the activity of the trionic transporter in the thick ascending limb of the loop of Henle (leading to an increase in the reabsorption of Na).

Increase in heart inotropism and chronotropism.

General vasoconstriction.

It is important to note that the Na reabsorption in the renal tubules is coupled with water reabsorption, this means that the increase in Na reabsorption also brings an increase in water reabsorption which in turn increases the total blood volume.

The increase in blood volume along with vasoconstriction, and increased inotropism and chronotropism lead to an increase in arterial blood pressure thanks to the increment in peripheral vascular resistance (vasoconstriction), the increment in the strength with which blood is pumped out of the heart (inotropism) and the increment in the frequency at which this blood is pumped (chronotropism).

Lastly angiotensin II also produces the liberation of aldosterone, the effects of these hormone:

Transcriptions of genes that lead to the expression of sodium channels.

Increase in the expression of sodium and potassium channels in the principal cells of the collecting and distal tubules (leading to an increase in Na reabsorption).

Increase in the expression of H+ ATPase in intercalated cells of the distal and collecting tubules (leading to an increase in Na reabsorption).

Increase in the activity of the Na/K pump (leading to an increase in Na reabsorption).

Summing up aldosterone increases Na reabsorption, K secretion and H+ secretion.

Then the RAAS is activated when a decrease in mean arterial pressure occurs and the combined actions of the hormones in the system result in an increase in the mean arterial pressure principally thanks to actions upon the reabsorption and secretion activities of the renal tubules in the kidneys.

Here is a picture summing up everything we have said.

For a PDF downloadable version of the above image: PDF version