Dopamine is a high yield topic. We give it four out of five. It is a natural hormone
and a neurotransmitter in the CNS and in the peripheral body. In the CNS it plays pivotal
roles in other high yield topics, such as Parkinson's Disease and Attention Deficit
Hyperactivity Disorder. It also is pivotal to the way that our brains perceive pleasure
and also the reward system in our brain. But that's not what we're talking about. This
lecture is going to be more about Dopamine as the adrenergic agonist, or Dopamine as
a drug. So, if you need more information on Parkinson's or some of those other diseases
of the Central Nervous System, you'll need to look those lectures up specifically. It
is a catecholamine, meaning that it has a benzene ring and two hydroxyl groups. Synthesized
from Tyrosine, but itself, it is actually an intermediate in the synthesis of Norepinephrine.
It acts on the Alpha 1, Beta 1, Dopamine 1 and Dopamine 2 receptors in the sympathetic
nervous system. Alright, now on to the mechanism of action and the effects of Dopamine. So,
we've already talked about what receptors are stimulated. We know that Dopamine 1, Dopamine
2, Beta 1 and Alpha 1 receptors are stimulated. This first bullet is talking about the affinity
of these receptors for Dopamine. So, Dopamine 1 and 2 receptors have the highest affinity
for Dopamine. And then Alpha 1 has the least affinity. And I'm really not even going to
cover what Dopamine 2 receptors do, just because it's low-yield for what you see physiologically.
Also, the Alpha 1 effect, that's kind of intuitive, so I mention that a little later, but I'm
not going to go into detail about what it does. I'm just going to focus on the first
Dopamine 1 and Beta 1 receptors. We have not talked yet, if you've followed the videos
sequentially, we have not talked yet about what the Dopamine 1 receptor is. Well, the
Dopamine 1 receptor acts post-synaptically to cause mostly a vasodilation of splanchnic
organs. What does this do? Well, this increases blood flow to the kidneys and also the gut
and other things. Why is that important? How does this compare to another presser that
we might use, such as Norepinephrine, because Dopamine is used as a presser. Norepinephrine,
it clamps down on everything, that's not necessarily a good thing. In cases of shock, we are oftentimes
worried about how much blood the kidneys are getting. Additionally, we a person comes in
in shock, their bodies are releasing a whole lot of Epinephrine in an effort to try and
increase their blood flow naturally. Well, this is a problem for the visceral organs
because it's still clamping down on the blood flow to them. However, because we can stimulate
the Dopamine receptor, we can bypass that system, and remember, Epinephrine works on
Alpha 1, Alpha 2, Beta 1 and Beta 2. It doesn't mess with the Dopamine receptors. Dopamine
bypasses that system, or bypasses those receptors, to dilate the kidneys, for example. Well,
that's great! That keeps the kidneys perfused. Next, Beta 1 stimulation. And we have covered
this before, if you have watched the videos sequentially, Beta 1 is going to cause an
increase in heart rate and contractility, increasing cardiac output and systolic blood
pressure - exactly what you would hope a presser does. Lastly, the receptor stimulation depends
on the dose. This is the same as Epinephrine, we've talked about a concept similar to this.
So, at low doses, you're going to see mostly Dopamine receptor physiology, and that just
means it's going to help dilate splanchnic organs. At mild, or medium doses, you're going
to see a Beta 1 effect. The contractility is going to go up, the heart rate is going
to go up, cardiac output is going to go up. Lastly, with very high doses, it's going to
look like a strong adrenergic response, or an Epinephrine response. You're going to see
a lot of clamping. Let's move on. Clinical uses and side effects of Dopamine. If you
look at the Clinical Uses, and you think it through, all three of those are pretty much
saying the same thing. We are helping to increase cardiac output. For the first one (Cardiogenic
shock) and the second one (Hypotensive shock) we are providing more blood to the brain,
we are providing more blood to the organs by increasing the cardiac output and clamping
down on the peripheries, but opening up the visceral arteries. And for the side effects,
that also kind of makes sense. We are stimulating the heart, we're asking it to do more work,
therefore, if someone is predisposed to Angina, it's going to cause Angina. It's going to
cause the heart to get a little bit hypoxic. And also, you could have the side effect of
cardiac arrhythmias, and that should also make sense if someone has a weak heart and
they are an elderly person, they could go into a disrhythmia. Knowledge Challenge: What
peripheral physiologic effect does dopamine have when given IV at low doses? The correct
answer is B. Change in renal arterial tone. We did talk about this, so you'll remember
at high doses, you'll see Alpha effects, at medium doses you see Beta effects and at low
doses, you see Dopamine receptor effects. What does that mean? Activating the Dopamine
receptors raises the cyclic amp levels in smooth muscle. This causes dilation in the
splanchnic organs and the kidneys. Low doses of dopamine are sometimes referred to as renal
doses because it increases renal blood flow. So, what happens when you increase renal blood
flow? What's going to happen to the GFR? Well, that's going to go up as more serum goes through
the kidneys, more urine is produced and more sodium is excreted. Alright, good job.