I'm reading conflicting info

Is there any vasodilators that you could like go to walmart to pick up? Could I mix a vasodilator with benzedrex to counteract negative effects?

I have come across such practice questions where they ask about function of bradykinin! And both these options are given! But In my view both are function of bradykinin!

Bernoulli's Principle and Vasodilation
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Question: So from what I understand vasoconstriction causes an increased blood pressure and vasodilation decreases blood pressure. This makes sense to me in the intuitive sense. However, from what I also understand of Bernouli's equation, this doesn't make sense. I'll try and explain with the vasodilation example. I feel as if one of these statements might be incorrect which is why I might be confused...

1. Vasodilation --> increased cross-sectional area
2. Increased cross-sectional area --> decreased velocity (A1V1=A2V2)
3. Decreased velocity --> Increased pressure (Bernouli's equation)
4. Therefore vasodilation --> increased blood pressure

Yet vasodilation is supposed to decrease blood pressure...

So I feel like I might be mistaken at either step 1 or step 3, but I really don't know where.. could you perhaps help explain this concept to me?

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Answer: First of all, all of the statements you provided there are correct when we're talking about physics. Vasodilation by definition means that we have an increased radius of small blood vessels due to one of many triggers. From the continuity equation, as you wrote, an increase in A, the cross-sectional area, will correspond to a decreased v, velocity. All else being equal (density of fluid, height, etc.), a decreased velocity corresponds to increased pressure.

And yet vasodilation does decrease blood pressure.

First, there are a number of assumptions that are true when we're talking about MCAT physics that don't apply in the human body:

1. The continuity equation assumes that the flow rate is constant; indeed, the very point of the continuity equation stems from the idea that if the flow is constant, then decreasing the cross-sectional area means the fluid has to come out faster. In biology, this is not necessarily true. In many cases, for example, vasoconstriction is caused by an outpouring of epinephrine (the idea being that in a fight-or-flight response, you don't want a bleeding risk and so the blood flow, especially to injured areas, decreases by vasoconstriction). At the same time, however, epinephrine increases heart rate and stroke volume. This leads to a much larger cardiac output, and therefore the continuity equation doesn't really apply. We're putting through a faster flow rate, so

My most annoying symptom is a difficulty tolerating water. Before I started taking nicotinic acid, and when I accidentally forget, I get horrible brain fog from drinking water, with or without electrolytes. My abdomen also slightly swells up with the fluid (ascites). And for some reason, even with a lot of extra water in my body, I don't produce much urine, it's always yellow instead of clear/dilute. The brain fog was so bad that I intentionally dehydrated myself, drinking less than a half cup of water a day, just to clear my head. The doctors all shrugged and told me to drink more water. But I found that nicotinic acid, the flushing form of niacin/vitamin B3, helps all that!

With the recent studies on long covid involving micro-clots in blood vessels, I have two ideas of what's been happening to my body. (1) Clots are blocking the blood vessels in my abdomen/kidneys, pushing fluid into my abdomen and preventing my kidneys from properly filtering out the extra water. (2) They're affecting my brain, and it's sending too many sympathetic nervous system signals/not enough parasympathetic signals, so the vessels down there are constricted and not letting blood through. (This is similar to POTS with blood pooling in the leg veins--I also have POTS symptoms.) Either way, the blood's not flowing.

Enter nicotinic acid. I first learned about it for long Covid with the hypothesis that it helps replenish NAD+/depleted biochemical precursors. But what I haven't seen mentioned is that it's a peripheral vasodilator, as evidenced by the flushing reaction. It relaxes and expands blood vessels. And it helps me feel my brain and live comfortably again!

Thoughts? Ideas?

I can't take any vasodilator (resveratrol, l-citrulline, Cialis) because I get headaches. I guess they are tension headaches but I'm not sure. I also take methylphenidate for ADHD which might have something to do with it.

Has anyone found a supplement or lifestyle technique to manage this problem?

New paper showing circulation issues post covid. What is everyone doing to improve circulation?

“The findings from the current study demonstrate that young otherwise healthy adults who continue to experience symptoms from COVID-19 beyond the acute phase of the illness exhibited peripheral vascular dysfunction. In contrast, vascular function appears to be restored in those who are no longer symptomatic. Furthermore, central arterial stiffness and cerebral vascular function were unaffected in subjects with COVID-19 beyond the acute phase irrespective of symptomology. Collectively, these findings highlight that the persistence of symptoms following COVID-19 is associated with peripheral vascular dysfunction in otherwise healthy young adults.”

https://journals.physiology.org/doi/full/10.1152/ajpheart.00368.2021?fbclid=IwAR2JHYIKmqjcLfPdUMauZlkoigctM-3PdmjdrwHCtlYzf4l8yjh628XNkJQ&

Hi all!

What vasodilators do you guys recommend from ND to stack with ADHD medication? I am thinking of the Ginkgo, any other ideas? Been having some ED from the medication vasoconstriction that needs solving.

Thanks

Hello,

Thank you for reading this. I was studying a topic on CVPhysiology.com, and came across this excerpt on factors influencing central venous pressure:

https://preview.redd.it/1fohfthx0zs71.png?width=1650&format=png&auto=webp&s=f8233d4cf4be6c486ab5a9c4b5c2bfbce4213c76

• I don't understand the highlighted text. Would greatly appreciate any help with that.
• Also, as a hypothetical, let's say that α-1 receptors only caused vasoconstriction of arterioles—not both arterioles and veins. now, would α-1 activation cause decreased central venous pressure?

Thank you.

hey guys, i’ve just been diagnosed with rosacea (skin disorder that causes uncomfortable red inflamed skin) and the past two times i’ve done acid my skin has reacted terribly, that i’m now on antibiotics for treatment. just wondering if there’s any kind of way i can reduce the amount of blood circulation to my face??? or if anyone else has experienced this?? ik this is stupid but it’s horrible ahahahah

Table 3: An overview of 5-HT receptors that are stimulated by psilocin. (Please click to zoom in)

Source

• Table 3 from Microdosing psychedelics: More questions than answers? An overview and suggestions for future research (PDF) [Jul 2019]

Further Research

>5-HT^(1A) receptor agonists are involved in neuromodulation. They decrease blood pressure and heart rate via a central mechanism, by inducing peripheral vasodilation, and by stimulating the vagus nerve.^([1])

• Further details in Table 1 from Serotonin as a Modulator of Glutamate- and GABA-Mediated Neurotransmission: Implications in Physiological Functions and in Pathology [Apr 2006] including malfunctioning pathologies, e.g. migraine:

Table 1: Serotonin Receptor Subtypes. 5-HT receptors have been grouped into seven principal classes, named 5-HT1 to 5-HT7; for each subtype, the table indicates the pharmacological characteristics, the localization, the intracellular action mechanism and final effect on neuronal excitability, the physiological function in which the receptor is involved and the pathologies deriving from its malfunctioning.

• Looking at the pharmacological/physiological effects of various serotonin receptors compared to the first table above - no psychedelics involved; this research^([2]) in the kidney of an anesthetized rat, show that 5-HT^(2) receptors are involved in vasoconstriction and 5-HT^(1/7) with vasodilation (the table above indicates 5-HT^(7) could be involved with vasoconstriction):

https://preview.redd.it/gw53l703g5j71.png?width=872&format=png&auto=webp&s=8e35bfeb365796e4bc67e27b3f9a677d2983ab4f

>Therefore, considering all these review, we can say that 5-HT is a potent vasoconstrictor substance in the kidney; but, unexpectedly, using different pharmacologica

I sometimes apply mirvaso (which is more of a gel consistency) and I also sometimes apply the brimonidine tartrate drops. They're definitely effective but it's kind of complicated. Sometimes I feel like their might even be a bit of a rebound flush effect. Or that it's effective but then if I get exposed to the sun or another trigger, my flushing is even WORSE if I've applied brimonidine tartrate.

i'm not sure which i prefer (drops or gel) even though I believe the gel is supposed to be stronger. The reason being I feel like the gel might also form too much of a layer on my skin and in a way clogging it up a bit or being it a bit warmer? which of course can trigger flushing

Anyway, it's a big complicated thing and there's def a psychosomatic element. I've dealt with it for years and i do believe having regrettably taken accutane as a teen and have a lot of chronic skin issues and discomfort still from that, makes it just this big "thing" and not just an unfortunate natural thing that some people just deal with.

I've started doing amazing with exercise, getting in the best shape of my life! i'm so proud of myself but sometimes this flushing issue flares up when I'm at the gym so I'm going back to the drawing board and seeing if there might be some additional tools or tricks to mitigate it, since I really want to protect this new fitness lifestyle I have.

Furthermore, I'm started a new job sometimes it flares up there, but I actually think at the gym is a bigger concern b/c my job doesn't really involve physical exertion so if it acts up I can kind of calm myself down but at the gym i basically need to stop working out so hard to combat it, which defeats the purpose of going.

In the past, I'd avoid the idea of another oral med but now that I'm a bit more education, I'm open to looking into some ideas.

What else is out there? I really want to be able to have a regimen where I can go to the gym and really go hard and not have to worry about the flushing.

I try to power through it but sometimes it gets so bad that people actually ask me about it or ask if i'm ok etc.

So far I like the effects of memantine, which I noticed after one dose. i'll post back later but the main thing i want to ask is if it's known to vasodilator and others experiences with those effects. i feel warm and see redness but it's too early for me to say if it is or isn't to an uncomfortable or problematic degree

10mg 2x daily (one AM and one PM is my prescribed dose for 20mg/day total)

For example, clenbuterol causes vasodilation and amphetamine causes vasoconstriction. Obviously, they're different compounds but what causes that?

I was 100% sure it was vasoconstriction (hence ACE inhibitors...), but a recent article from NIH oddly says “When angiotensin I is converted to angiotensin II, it has effects on the kidney, adrenal cortex, arterioles, and brain by binding to angiotensin II type I (AT) and type II (AT) receptors. The effects discussed below are a result of binding to AT receptors. The role of AT receptors is still being investigated, but pertinently, they have been shown to cause VASODILATION by nitric oxide generation.” [Source: https://www.ncbi.nlm.nih.gov/books/NBK470410/]

Am I missing something here? Was this a typo? I don’t think so, because apparently other sources also affirm that AT receptors do indeed cause vasodilation, which makes no sense to me. The rest of the NIH article then went on to describe how the effects of these receptors cause vasoconstriction/high blood pressure...

Any help or clarification is appreciated!

Do ace2 receptors come back? Do enough get destroyed? Why do long haulers recover? Is that ace2 functionality restoring? Does covid downregulate ace2 in the short term and cause the body to upregulated in the long term?

Can I rub my face on my cat to stimulate a histamine response via allergy as a budget preworkout?

Despite my limited knowledge and the method's own flaws, I know that a type of fMRI analysis measures blood flow, and we say that if there is more flow to one part of the brain, then that part must be more active. But there is something that controls this flow, isn't there? And we think of the prefrontal cortex as the 'executor' of the brain. So wouldn't the executor then have a role in controlling blood flow, or is vasodilation purely a sympathetic reaction?

Asked in another way: When I think about a pink elephant, is blood flowing to my visual cortex a sympathetic reaction from increased activity that occurs after maybe a resource demand, or are vessels dilated maybe in anticipation or in preparation for activity?

And in any case, do we know what controls it?

*Edited after thinking for a bit
*Edited for grammar

I’m interested in taking quercetin for my histamine issues and overall health. I’ve read that it can have a vasodilation effect. I react very poorly to any kind of vasodilating compound (coq10, beetroot). Has anyone whose used quercetin experienced this effect? Did it trigger pots symptoms?

So in preparation for the side effects I’m planning on cold (distilled) water extracting with Lemon Juice and a Garlic Clove then taking Turmeric and Magnesium capsule and Crystallized Ginger as needed. Also have dark chocolate 10mg thc each. Also gonna trip in bed with backyard within walking distance if I gotta puke or look at the sky. I will be getting two tabs of LSD soon so I’ll have to see how high dose compares to a high dose of LSA.

Hello I am very confused about vasoconstriction and vasodilation and blood pressure and how it applies in certain cases. For example, I know that angiotensin II causes vasoconstriction in order to increase blood pressure. With the end goal of aldosterone being to increase blood pressure, that makes sense to me. What I don't understand is how would that help if a constricted afferent arteriole caused a decreased hydrostatic pressure in the glomerular capillaries? Wouldn't more vasoconstriction just cause even more of decrease in blood reaching the glomerular capillaries? Another example of my confusion is with the response of the autonomic nervous system. Say during the sympathetic response you need to divert blood from the digestive organs to organs that are more important for this response, like the brain. Would your body vasoconstrict to increase the blood pressure or would you vasodilate because this increases blood flow?

I guess another issue is I don't understand the difference between blood flow and blood pressure beyond the definitions. I get that blood flow is the force that blood exerts on the vessel walls and blood flow is the movement of blood through the walls but beyond that I don't get which one is more "important"? (Not really the right word for it but I hope you get what I mean)

As you can see I do not have a good grasp on this concept so any help is appreciated!

the half-life of allicin which is responsible for it is less than 1 minute. It becomes the mercaptan allyl. That is, the blood-dilating effects of Allycin increase blood pressure and decrease blood pressure. They only last a few minutes? Does it look any different?

Last time I noticed a stuffy nose when coming up on morning glories. I notice it again this time. That is when some of the flesh in the nose swells up and makes breathing through the nose more difficult, not when it's clogged by secretion.

This is weird because people talk about vasoconstriction from morning glories. But isn't this vasodilation? I mean the blood vessels widen and let more blood into that tissue. Decongestant medications cause vasoconstriction to undo this.

In my head kinda having a problem processing these.

So vasoconstriction will increase the pressure and velocity, but decrease the flow rate (cardiac output), cross-sectional area, and the amount of blood it can carry.

Vasodilation will decrease the pressure, and velocity, but increase the flow rate (cardiac output), cross-sectional area, and the amount of blood.

How is that cardiac output (flow rate => Q=AV) increase when it is vasodilated but the velocity decreases and vice versa?

Thanks.

So when inflammation or a injury happens, our blood vessels goes to vasodilation to make more white blood cells, coagulation factors or proteins to get in the injury area. And that makes total sense.

Also our blood vessels goes to vasoconstriction to reduce the blood flow, so that way lesser blood will be lost due to hemorrhage. And that makes total sense too.

I am confused here, so both vasoconstriction and vasodilation happens when inflammation happens? Surely this doesn't make any sense. What am I missing?

So I thought that vasoconstriction causes an increase in blood pressure. But I’m confused because in the answer explanation for question 4 on the section bank, it says that “increases in blood pressure result in vasoconstriction, not vasodilation.” Can anyone explain this discrepancy?

I was 100% sure it was vasoconstriction (hence ACE inhibitors...), but a recent article from NIH oddly says “When angiotensin I is converted to angiotensin II, it has effects on the kidney, adrenal cortex, arterioles, and brain by binding to angiotensin II type I (AT) and type II (AT) receptors. The effects discussed below are a result of binding to AT receptors. The role of AT receptors is still being investigated, but pertinently, they have been shown to cause VASODILATION by nitric oxide generation.” [Source: https://www.ncbi.nlm.nih.gov/books/NBK470410/]

Am I missing something here? Was this a typo? I don’t think so, because apparently other sources also affirm that AT receptors do indeed cause vasodilation, which makes no sense to me. The rest of the NIH article then went on to describe how the effects of these receptors cause vasoconstriction/high blood pressure... ?

Any help or clarification is appreciated!

I’m interested in taking quercetin for my histamine issues and overall health. I’ve read that it can have a vasodilation effect. I react very poorly to any kind of vasodilating compound (coq10, beetroot). Has anyone whose used quercetin experienced this effect? Did it trigger pots symptoms?

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So does vasoconstriction increase blood pressure and does vasodilation decrease blood pressure. Also how does this work with the Venturi effect? If the cross sectional area is lower does that mean increased velocity and increased blood pressure?