This doesn't make sense. Alpha 1 receptors in the kidney inhibit renin release, the same renin that is a part of the RAA system, one of the most powerful VASOCONSTRICTIVE mechanisms our body has, and yet Alpha 1 stimulation causes overall vasoconstriction? That would mean our body is ineffeciently working against itself, something I have yet to see. And this is separate from the negative feedback mechanism.
If alpha 2 receptor activation leads to decreasing the release of neurotransmitters from the synaptic vessels by negative feedback mechanism. then it ultimately leads to decrease in the sympathetic response right. then how can you say the drugs (Alpha 2 receptor agonist) classified under adrenergic agonist. though they are decreasing the adrenergic or sympathetic response by decreasing the neurotransmitter release
Great job, All your videos are great, only if you can put the slides in the description in youtube, or if you can attach it on fb, so we can download it and print it, that would help us so much, also You should allow people to donate to the channel.
Guys, I’m only 14, so give me a break for asking this. But what is catochlomine?! I have this medical book and it mentions it 100000000 times but never explains what it is or what it does, and I can’t find it in this video. Plz help!
Highly intellectual and excellent video. Done very diligently and in a very clear way. Easy to undersand. Perfect to study for Pharmacology exams. Studying from it for todays exam. Thank you so very much for taking your time and making this excellent video.
why does alpha 1 receptor inhibits renin release?in fight or flight response, i believe that one's blood pressure would shoot up due to rise in renin release and also vasoconstriction of the vessels, right?
At interval 5:02 you said that kidney contains a1 receptors which stimulates release of renin but in actual all the tissues to be stimulated have a1 receptors but not heart , JGA in kidney and adipocytes they contain b1 adrenergic receptor ..... b1 receptor in kidney stimulates release of renin not a1.....
no... they found on the both adrenergic & cholinergic post ganglionic neuron. but when it comes to the effector site, it changes. adrenergic neurons have Alpha and beta receptors, while cholinergic neurons have muscarinic receptors
"Specific beta(2)-agonist effects on the pancreatic beta cell result in increased insulin secretion, yet other mechanisms, such as increased glucagon secretion and hepatic effects, cause an overall increase in serum glucose and an apparent decrease in insulin sensitivity." J Allergy Clin Immunol. 2002 Dec;110(6 Suppl):S313-7
I was having a hard time understanding the difference between epinephrine and norepinephrine. It's always been explained to me in a complicated way and it turns out the difference is so simple. Thank you for breaking it sown for me!
You forgot abt beta 2 receptors that they also r present on liver and cause gluconeogenesis and glycogenolysis thus increasing blood glucose level ... and also cause increase in intracellular potassium intake...
Thank you very much from a second semester, nursing student. I know there are certain classes that people dread (pharmacology, anatomy and physiology, medical terminology, microbiology). But for me, if I can visualize the concepts into some sort of story, I'm golden. Thanks for helping me be able to visualize this.
Thank you for this video. So you are saying that out of the drugs that you presented, Dopamine, NE, and E are catecholamine like and have a short half-life, while the rest like ephedrine, phenylephrine, dobutamine, etc are non-catecholamines and thus has longer duration of action?
Antidepressants are medications that can help relieve symptoms of depression, social anxiety disorder, anxiety disorders, seasonal affective disorder, and dysthymia, or mild chronic depression, as well as other conditions.
They aim to correct chemical imbalances of neurotransmitters in the brain that are believed to be responsible for changes in mood and behavior.
Depression Medications (Antidepressants)
These are the most commonly prescribed type of antidepressant.
Serotonin and noradrenaline reuptake inhibitors (SNRIs) are used to treat major depression, mood disorders, and possibly but less commonly attention deficit hyperactivity disorder (ADHD), obsessive-compulsive disorder (OCD), anxiety disorders, menopausal symptoms, fibromyalgia, and chronic neuropathic pain.
SNRIs raise levels of serotonin and norepinephrine, two neurotransmitters in the brain that play a key role in stabilizing mood.
Selective serotonin reuptake inhibitors (SSRIs) are the most commonly prescribed antidepressants. They are effective in treating depression, and they have fewer side effects than the other antidepressants.
SSRIs block the reuptake, or absorption, of serotonin in the brain. This makes it easier for the brain cells to receive and send messages, resulting in better and more stable moods.
They are called "selective" because they mainly seem to affect serotonin, and not the other neurotransmitters.