Which hormone increases blood pressure by vasoconstriction?

Vasopressin (arginine vasopressin, AVP; antidiuretic hormone, ADH) is a peptide hormone formed in the hypothalamus, then transported via axons to the posterior pituitary, which releases it into the blood.

AVP has two principle sites of action: the kidney and blood vessels.

1. The primary function of AVP in the body is to regulate extracellular fluid volume by regulating renal handling of water, although it is also a vasoconstrictor and pressor agent (hence, the name "vasopressin"). AVP acts on renal collecting ducts via V2 receptors to increase water permeability (cAMP-dependent mechanism), which leads to decreased urine formation (hence, the antidiuretic action of "antidiuretic hormone"). This increases blood volume, cardiac output and arterial pressure.
2. A secondary function of AVP is vasoconstriction. AVP binds to V1 receptors on vascular smooth muscle to cause vasoconstriction through the IP3 signal transduction pathway and Rho-kinase pathway, which increases arterial pressure; however, the normal physiological concentrations of AVP are below its vasoactive range. Studies have shown, nevertheless, that in severe hypovolemic shock, when AVP release is very high, AVP does contribute to the compensatory increase in systemic vascular resistance.

There are several mechanisms regulating the release of AVP, the most important of which are the following:

1. Hypovolemia, as occurs during hemorrhage and dehydration, results in a decrease in atrial pressure. Specialized stretch receptors within the atrial walls and large veins (cardiopulmonary baroreceptors) entering the atria decrease their firing rate when there is a fall in atrial pressure. Afferent nerve fibers from these receptors synapse within the nucleus tractus solitarius of the medulla, which sends fibers to the hypothalamus, a region of the brain that controls AVP release by the pituitary. Atrial receptor firing normally inhibits the release of AVP by the posterior pituitary. With hypovolemia or decreased central venous pressure, the decreased firing of atrial stretch receptors leads to an increase in AVP release.
2. Hypotension, which decreases arterial baroreceptor firing, leads to enhanced sympathetic activity that increases AVP release.
3. Hypothalamic osmoreceptors sense extracellular osmolarity and stimulate AVP release when osmolarity rises, as occurs with dehydration.
4. Angiotensin II receptors located in a region of the hypothalamus regulate AVP release – an increase in angiotensin II simulates AVP release.

Heart failure is associated with what might be viewed as a paradoxical increase in AVP. Increased blood volume and atrial pressure associated with heart failure should decrease AVP secretion, but it does not. It may be that sympathetic and renin-angiotensin system activation in heart failure override the volume and low pressure cardiovascular receptors (as well as the hypothalamic control of AVP release) and cause an increase in AVP secretion. Nevertheless, this increase in AVP during heart failure may contribute to the increase in systemic vascular resistance as well as the enhanced renal retention of fluid that accompanies heart failure.

AVP infusion is sometimes used in treating septic shock, a condition that can be caused by a bacterial infection in the blood and the release of bacterial endotoxins such as lipopolysaccharide. Infusion of AVP increases systemic vascular resistance and thereby elevates arterial pressure. Some studies have shown that low-dose infusions AVP (which are used in septic shock) also cause cerebral, pulmonary and renal dilation (mediated by endothelial release of nitric oxide) while constricting other vascular beds.

Reference:  Den Ouden, DT and Meinders, AE. Vasopressin: physiology and clinical use in patients with vasodilatory shock: a review. The Netherlands Journal of Medicine 63:4-13, 2005

Revised 12/8/16

DISCLAIMER: These materials are for educational purposes only, and are not a source of medical decision-making advice.

Video transcript

We left off the story of antidiuretic hormone when it was just secreted into the blood vessels of the posterior pituitary. So it was just synthesized, just made. It's a little hormone. And ADH was on its way to different parts of the body. So let's just pick up the story right there. And figure out where does it go next. So this little molecule is, we said, a small peptide hormone made up of amino acids. And so I'm just going to draw it here. And this little hormone is going to go off to do a couple of important things. So we know at the end of the day, it really wants to increase blood pressure. So one of the places it visits is all of the vessels of the body, all the arterial vessels of the body. And specifically, it targets smooth muscle. So this hormone is going to go and get this smooth muscle to constrict. And we know that when smooth muscles constrict, the blood vessels are actually going to tighten down, and we call that vasoconstriction. So the blood vessels are going to get tight and small, and that's going to increase resistance. And increased resistance is going to relate to blood pressure. And we'll talk about how we know that. There's that formula. I'm going to write it over here-- delta P equals flow. Q is flow times resistance, is R. And you can actually change that around to say arterial pressure minus venous pressure equals-- and we know the flow is actually stroke volume times heart rate, and it's all multiplied by resistance. So if you look at this, and if we assume for the moment that the venous pressure is going to be basically unchanged, then anything that increases the resistance over here is going to increase our pressure over here. So that's why, in this case, if ADH is able to cause constriction of the blood vessels and increase resistance, our pressure would go up as well. So that's actually one of the things that it does. And the other thing that it does is it's going to act on the kidney. So it's going to have an effect on the kidney. Here's my kidney. And specifically what it's going to do is it's going to cause increased reabsorption of water. So increased reabsorption of water is going to increase our stroke volume. So now you can see the other key effect it's going to have. If it's going to cause your stroke volume to go up, then just as before, now you have an increased stroke volume. So your arterial pressure is going to go up, maybe doubly up. So it's going to cause the blood pressure to go up for a couple different reasons. Now, let's explore this second point in a little bit more detail, the whole idea of how it causes the stroke volume to go up. So for that, what I want to do is I'm actually going to create a little bit of space. And I'm going to draw out, again, as I've done before, the efferent and afferent arteriole. So we know that blood is going to enter the kidneys, and it's going to do this twisting on itself in the glomerulus. And so this is our little glomerulus. And there's the proximal convoluted tubule. And there's the loop of Henley. And this is the distal convoluted tubule, and finally, a collecting duct. So we know that this is basically what the nephron looks like. And I haven't label all the parts, but I'm going to label the important part, which is this part right here. So this area here is the collecting duct. And what I'm circling in blue is what the ADH is actually going to work on. It's going to work on this area, the collecting duct. So it's going to have its effect here specifically. And let me try to draw this a little bit larger so we can see exactly what goes on. So let's imagine that you have, let's say, one cell there. And here's another cell here, something like that. And you have a blood vessel going alongside of it. Now, we haven't actually talked about this before. But down in here-- actually, let me switch colors for a moment. We have urine going this way, and blood going this way. So already, you might be a little surprised. You're thinking, well, why is blood going up and urine going down? That makes no sense. Now, think about this. Before when we were talking about blood and urine flowing in other parts of the nephron, we were kind of separating out the nephron, talking about this top bit. So we were talking about this top bit here. And in here, the concentration is around 300. And actually, the units on that-- I'll just write the units up here-- are milliOsms. So it was around 300, but if you go deeper, it's about 600. And then if you go deeper than that, it's about 900. And if you go down here, it's about 1,200. So what's happening as you go deeper is that it's basically getting more and more salty. So it's getting very salty. I'll actually write that sideways, very salty as you go down. And that saltiness is really, really important, because what it does is it allows us to concentrate our urine. And you'll see why I say that. So keep that saltiness in mind and the fact that there's this big gradient. And I'm going to actually just assume, right now, that we're talking about something, let's say, at the 900 level. So we're at this point right here-- 900 milliOsms. So we've got a pretty salty area out here. Now, as I said, urine is flowing through. And in these collecting duct cells, we have something called an aquaporin that basically sits like this. Let me actually show you what it would look like. So these areas are not going to allow water to go through. That's actually the first point that I want to make. Water cannot go through these areas, except for when there's a little aquaporin channel. And I'm drawing the channels for you. So you can see they're not on the surface, right? So there's no way that water, if water is sitting over here, there's no way that it can actually get through. It would actually just bounce off because it's not able to permeate the cell. It can't actually get in. So water just kind of bounces back and basically goes down into the urine. Now, what ADH does-- and this is the neat thing. So ADH, what it will do, is it will float up. So ADH is actually going to float through the blood, because we said that ADH is going to be all over the body. So this little molecule is going to go through and float by this collecting duct cell. And it's going to have an effect on it. So it's going to have an effect on this collecting duct cell. What it's going to do exactly is it's going to make those little aquaporins. Let me write that out actually. This is an aquaporin. And you can see that's a really easy word to remember because it's literally aqua, meaning water, making a pore for water. So this aquaporin vesicle is actually going to merge with the wall. It's actually going to merge with the wall like that. So let me actually erase a little bit and show you what would happen. So now you have-- instead of this aquaporin sitting out here, you literally have little channels that are now fused in with the wall. So you can see how those little vesicles just bumped right into the wall and fused into it. And now water is going to get a free ride across. It's going to be able to just go right through that channel just like that-- boop-- and into the blood. And it's going to do it again here. And it's going to go here. So all this water is just gushing in to the blood. Look at all this water. And so this blood is going to be loaded with water now, something that it did not have before, because the water couldn't get across before. And so this blood is going to go up, loaded with water, because of the ADH. The ADH basically allowed all that water to finally get across, and the blood is now full of water. +And so now you can see how the volume of blood is going to go up. And if the volume of blood goes up, it's going to create a larger stroke volume for the heart. So that's specifically how the stroke volume goes up.

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