Not THAT “other brain”.
It is sometimes said that the kidneys are a human body’s “second brain”. They do have an awful lot of work to do. You probably already know that the adrenal glands on top of the kidneys are responsible for secreting a number of very important hormones. You also know now that the nephron is the functional unit of a kidney, and that is where all the fun electrolyte action happens.
But did you know that the nephron itself excretes a hormone that culminates in vasoconstriction? This is one way that the kidneys compensate for low blood pressure or blood volume. The hormone is called renin, and it is awesome.
The Renin-Angiotensin-Aldosterone System (sometimes just called the Renin-Angiotensin system, or RAAS) is a chemical pathway. Much like the metabolic pathways in your liver, RAAS consists of several substances converting into others through the action of enzymes.I love RAAS because it kind of thwarts the notion of separate organ systems, and just barges through four of them. Stick it to the man, RAAS! Here is how it works:
The glomerulus is the knot of capillaries that begin the process of filtration in the nephron. Nearby, the juxtaglomerular cells carefully monitor the rate of blood flow into the tubule. One of their main functions is to secrete renin in response to slowed blood flow. This can be due to any number of things, but the kidneys “know” that they won’t be able to work properly without the right amount of filtration.
Once renin is released, it meets up with an inactive substance secreted by the liver, called angiotensinogen. (Just a quick aside, when you see that the name of a compounds ends in -inogen, it usually means it is an inactive precursor. Something else has to cleave it or add to it to make it active!) Renin cleaves (cuts off) a part of angiotensinogen, turning into the now active Angiotensin I.
Angiotensin I then meets up with an enzyme called, creatively, Angiotensin Converting Enzyme (ACE). ACE turns Angiotensin I into Angiotensin II. It is generally agreed that this process happens in the lungs, but that agreement will likely be turned on its head eventually, so let’s just assume for now. Although it is theorized that Angiotensin I has some effective properties of its own, our general concern here is with the effects of Angiotensin II, as they are quite varied.
Angiotensin II does a bunch of stuff. I’ll just go ahead and list some of it:
1) Causes the blood vessels to constrict, especially those that lead to the nephron. This allows the rate of filtration at the glomerulus (GFR) to remain constant even though there is less blood flow.
2) Signals the release of antidiuretic hormone (ADH aka vasopressin) from the posterior pituitary gland.
3) Signals the release of aldosterone from the adrenal gland.
The net effect of this system is a rise in blood pressure. Antidiuretic hormone and aldosterone both hold on to water and electrolytes, keeping up the blood volume. Vasoconstriction maintains the GFR. The kidneys, once again, are happy.
But…what if the reason you have a reduced filtration rate is due to reduced cardiac output? What if your heart is not getting enough oxygen and is not working its best as a pump? Do your kidneys, those little second brains, know this?
All they know is that not enough blood is getting to them. So this compensation mechanism, as long as there is reduced cardiac output, will continue to vasoconstrict and hold water and salt. This compensation mechanism will definitely reduce the amount of oxygen that is able to get to your heart when it needs it. So you can see how this might be bad news for someone prone to a heart attack.
Lucky for us, pharmacology has a couple of tools to help us overcome this little snag.