I learned something interesting at orientation today at my new per diem job today - renal stent placements had a profound effect on lowering hypertension. The person that told us this wasn't able to elaborate on this at the least, unfortunately. I'm wondering who on this forum knows any details on this procedure.
Renal Stents
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JPINFV
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Lower renal blood pressure (such as after a kink in the line, so to speak) increases the amount of renin secreted from the juxtaglomerular cells. Renin converts angiotensinogen to angiotensin 1. Angiotensin 1 then moves to the lungs where it is converted to angiotensin 2 by the angiotensin converting enzyme (hence ACE inhibitors. -pril drugs). Angiotensin 2 is both a vasoconstrictor and stimulates the release of aldosterone from the adrenal glands. Aldosterone works by stimulating the kidneys to increase water and sodium reabsorption, which also works to increase blood pressure and blood volume.
8jimi8
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I've always seen it described as a "potent vasoconstrictor," in textbooks
So the first thing to realise here, is that renal stenting is going to help a subset of patients with secondary hypertension due to renal artery stenosis. The vast majority of hypertensive patients (90-95%) have primary hypertension --- meaning that while we know they're hypertensive, and there's a lot of competing theories as to why that is, there's not one single well-defined and understood mechanism.
There's an article about this here at medscape:
http://www.medscape.com/viewarticle/409069_4
One of the methods used to generate hypertension in experimental animals is to clamp the renal artery.
There's an article about this here at medscape:
http://www.medscape.com/viewarticle/409069_4
One of the methods used to generate hypertension in experimental animals is to clamp the renal artery.
I'm familiar with the renin-angiotensin system. So what you're saying is, if that lowered renal BP is resolved by placing the stent, renin prouction will decrease markedly, and along with it a significant decrease in the pt's BP, correct? Score one for western medicine, for actually treating the cause rather than simply medicating for symptomatic care. Renal stent placement would be much more preferable than getting a script for ACE inhibitors, I would think.
Have renal stent placements been a widespread practice, or is this a relatively new procedure? This is the first I've heard of it.
Is it possible to Dx renal artery stenosis, or are they just guessing?
It looks like it can be measured with contrast angiography, CT, doppler ultrasound, etc. Here's a free text article I found that also talks about some other causes of secondary hypertension.
http://www.hellenicjcardiol.org/archive/full_text/2010/6/2010_6_518.pdf
Unfortunately only around 1-5% of hypertensive patients have a renovascular cause.
I have to admit that this isn't something I know a lot about -- perhaps one of the med students or physicians on the forum might have relevant experience?
Depends on what you mean by profound.
AT II affects bp in several ways, one of which is a vasoconstrictor.
However, locally, endothelin and TXa2 are very powerful. Probably more so than angiotensin.
abckidsmom
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Is there any way to measure that? I didn't quite realize TXa2 was that much of an influence. Makes sense, of course, but It's not anything I'd previously thought about.
It is a vascular surg pathology and treatment, it has been around a while.
Like other surgical procedures, they are not always indicated and there are alternatives. Sometimes it doesn't help at all.
In secondary HTN, which as pointed out earlier, is a minority, renal occlusive disease is one cause.
In addition to a stent, which is not always possible, because of the morphology of the plaque, Endarterectory is also possible.
I have seen renovascular occlusive disease most often discovered during endovascular procedures for other pathology. Which is one way to find it.
If it is primarily suspected, dopler ultrasound is the cheapest test. Ace Inhibitor challenge, (once you make sure there is more than 1 functioning kidney with USG) is also a cheap and easy test, but not a first line.
MRI and radionucleotide scanning are the more expensive of the diagnostic images.
I would think there is a way to measure it and considering that in all the textbooks the effects are often described in molecular detail.
Those mediators are produced in endothelial tissue, and are responsible for the vasoactive control of hemorrhage.
Elevated TXa2 can also shut down placental circulation, not something seen often with ATII. (I have never seen or heard of ATII doing that)
It is also inhibition of TXa2 that helps protect females from various vascular pathologies during reproductive years. The main physiologic purpose of increased inhibition TXa2 in females is specifically for spiral arteries in placental circulation.
I apologise for the long post that follows.
* It depends partially on how you define powerful. Often we consider the power of a substance in terms of potency, i.e. if I can get the same analgesic effect with 100ug fentanyl as 10mg morphine, as 75 mg demerol, many people would conisder fentanyl to be more powerful than morphine, and morphine to be more powerful than demerol. This is an issue of potency, and in terms of potency fentanyl > morphine > demerol. Perhaps a more relevant consideration when judging power is to look at maximal effect. In this case, we know that if we give large enough doses, fentanyl and morphine have about equivalent ability to reduce pain. In constrast, demerol is a weaker analgesic than either morphine or fentanyl, even in large doses. So, from this perspective, it might be reasonable to say that morphine and fentanyl are equally powerful, but demerol is less powerful.
* It's hard to do this in humans. If you're developing a pharamaceutical product, like a new ATII blocker, or an agent directed against TXA2, etc. part of the long clinical trial process is going to be determining dosing. So you might work out what the maximal effect or the potency of an agent is. If you see a greater effect with an agent that blocks TXA2 than one that blocks ATII, you might conclude that one or other has a larger effect in vivo in humans. But this could just reflect one blocker being more effective at its target.
* So typically you have to go to small rodents, which is what you'll mostly find on pubmed. And now you're comparing a 35g mouse, or a 300g rat to a 70kg human. Often these comparisons are valid, but sometimes they're not. Hence the long clinical trial process for any new drug.
* You can give substance X to a rat, for example, and measure the change in blood pressure that results. But this is an indirect measure of the effect of the compound on vasoconstriction, as blood pressure depends on SV and HR as well as PVR. Typically drugs are given to these animals by intraperitoneal injection (i.e. into the peritoneum). This is painful, and causes the rat's heart rate and blood pressure to go up, complicating analysis. Any method that involves restraining the animal, e.g. using a tail cuff, or having an arterial line sutured out of the back of the neck while the animal is conscious, causes additional stress. Alternatively you can do these experiments under anesthesia, but then you risk seeing the effect of whatever agent you're using for anesthesia on blood pressure, e.g. isoflurane, ketamine, pentobarbitol. Another option is to operate an animal, and place a radiotransmitter connected to an arterial line in the abdomen, and a drug pump. This avoid anesthesia and restraint stress, but still gives you the risk of an animal with a subacute infection that may also be hypovolemic.
* A direct way of measuring how a substance affects vasoconstriction is to kill a rat / mouse, take out a ring of blood vessel, and mount it on a tension-measuring device called a myograph. You suspend this in a physiologic salt solution bubbled with CO2 and O2, that mimics tissue conditions, then you give doses of whatever compound you're interested in and measure the force generated by the muscle contracting. This is a direct measurement, but is less physiologic, as the tissue is no longer in a living organism.
* There's also an option to do various pharamcological tests where you assay how the drug target, e.g. the receptor, binds the substance of interest. But this doesn't tell you about the magnitude of the effect produced by binding.
* It's also possible to produce animals that make too much of a given substance, e.g. a mouse overexpressing genes necessary to produce angiotensin II, e.g. angiotensin converting enzyme ---- or animals that make none, or too little, or lack the relevant receptors, or have too many of the receptors, or receptors that continuously signal, and so on. Then you extrapolate this data.
Lots of patients are on ACE inhibitors or ARB antagonists, but probably only 10% or so of these patients have renal artery stenosis. There's a lot of "chicken or the egg" diagnosis and treatment involved with hypertension. Hypertension from one cause causes some vasoconstriction, which kicks up the renin-angiotensin-aldosterone system, which causes increased blood volume and/or pressre to maintain flow which further worsens hypertension, yada, yada, yada. That's why you see so many patients on a cornucopia of different medications, all to treat hypertension, but all treating a different piece of the puzzle. Simply treating a single cause of the disease explains why a lot of patients aren't well controlled and why we're seeing more patients on a variety of medications. Of course weight loss, exercise, and stopping smoking would go a long way in many of these patients as well.
Renal artery bypasses were quite common in the past and are still done in some cases. Angioplasty and stenting has decreased the need for bypass surgery significantly, just as they have in the cardiac arena.