00:00
Antidiuretic Hormone or Arginine Vasopressin. This molecule will also increase blood pressure and
it does it through another mechanism. Angiotensin II directly stimulates its release.
00:17
Hyperosmolality which means a high plasma osmolality will also stimulate its increase. If there is
sympathetic stimulation that will also stimulate arginine vasopressin antidiuretic hormone to be
released. It is released from the posterior pituitary and will bind to a couple of systemic
receptors. V1 receptors are located on blood vessels and that will cause vasoconstriction.
00:48
Remember vasoconstriction decreases tubuloluminal diameter which increases resistance
which then increases arterial blood pressure. V2 receptors are located in the collecting tubules
and this helps with water or fluid reabsorption. This increases blood volume and it is blood
volume then increasing preload, increasing cardiac output will then increase arterial blood
pressure. So another way to respond to a decrease in arterial blood pressure is by releasing
antidiuretic hormone or arginine vasopressin. Another neurohumoral factor is natriuretic
peptides. Natriuretic peptides are going to work in opposition of some of the other things like
the renin-angiotensin-aldosterone system that has been discussed previously. Atrial
natriuretic peptide has its own items or stimulatory factors that allow it to be released. They
respond to atrial distension which means how much stretch is done to the atrium, that's the
right or the left atrium. Sympathetic stimulation also stimulates its release. Angiotensin II and
endothelin. All are stimulatory factors for ANP. Probably the most important of these though is
atrial distension. So if you have a distended atrium, it means that too much fluid went into it.
02:40
It stretched it too much. So how are you going to respond to too much stretch? Well, one
reason could be there's too much blood volume in the system. So maybe you want to get rid of
blood volume and that is one of the things that ANP will try to do. So ANP acts directly on the
kidneys in a couple of ways. One is by changing glomerular filtration rate and renal blood flow
and the other is acting in the opposite form as what the renin-angiotensin-aldosterone system
does. So remember that renin usually stimulates ang II and aldosterone. ANP decreases renin
release which decreases ang II, which decreases aldosterone. All of these factors work
together to cause two things, sodium loss which is natriuresis and water loss which is diuresis.
03:42
If you lose sodium and you lose water, you're going to decrease your blood volume. As blood
volume falls, so will central venous pressure so will cardiac output and therefore you decrease
arterial blood pressure. There are also some minor effects that ANP have directly on blood
vessels but these are fairly minor but they will have some effects in certain conditions that will
eventually also help to decrease central venous pressure and maybe decrease systemic
vascular resistance slightly but again these are minor effects but the same overall effect
happens and that is a decrease in arterial blood pressure. Atrial natriuretic peptides, we talk
about their main stimulates for release is stretch, sympathetic stimulation and angiotensin II
and endothelin. Brain natriuretic peptide is something we also have to discuss. It's part of the
natriuretic peptide family. Brain natriuretic peptide is released by the ventricles so this is the
right and left ventricle. In response to the same things, stretch, sympathetic stimulation, ang II
and endothelin. The reason why we talk about brain natriuretic peptide separately is because it
has a very good diagnostic marker for heart failure. So in heart failure you have a volume-
overloaded condition. Therefore, you have too much volume in the system. Blood volume is too
high. How does the body respond to that? By trying to get rid of that volume and it does that
through ANP and BNP but it just so happens that natriuretic peptides are not that potent. They
work but they aren't as potent as the renin-angiotensin-aldosterone system. If the RAAS
system is working, it will override the natriuretic peptides but you can track the natriuretic
peptides to see how much volume overload is occurring in the heart failure patient. So
oftentimes people will not just look at ejection fractions but also brain natriuretic peptide levels
for people in heart failure to see if their medications are working correctly. So this is a nice
diagnostic marker as part of the overall natriuretic peptide system.