How does sodium affect your blood pressure?
June 23, 2006 6:46 AM Subscribe
What in the process of absorbing sodium causes an increase in blood pressure
What in the process of absorbing and incorporating sodium into the human body actually causes an increase in blood pressure and/or heart disease?
Is it constricting blood vessels?
Is it change in heart beat?
Something else?
What in the process of absorbing and incorporating sodium into the human body actually causes an increase in blood pressure and/or heart disease?
Is it constricting blood vessels?
Is it change in heart beat?
Something else?
From the (very!) little I know about medicine, salt is absolute necessary to hydration. If you're dehydrated, it doesn't matter how much pure water you drink... it won't 'stick' without salt.
Presumably, this can work in reverse... if you have high sodium intake, you'll tend to retain more fluid, and your blood pressure will be higher. I think that's the theory, anyway. Possibly disproven, per docpops.
posted by Malor at 7:21 AM on June 23, 2006
Presumably, this can work in reverse... if you have high sodium intake, you'll tend to retain more fluid, and your blood pressure will be higher. I think that's the theory, anyway. Possibly disproven, per docpops.
posted by Malor at 7:21 AM on June 23, 2006
docpops writes "I'm not sure there is really ongoing support for the notion that sodium increases blood pressure universally. I think retrospective trials have shown that certain persons are more sodium sensitive and others aren't. That said, my abysmal recall of first year med school physiology is that as sodium levels rise in the bloodstream water balance favors absorption back into the vascular system to maintain a constant osmotic pressure, thus increasing blood pressure."
I realize there's doubt that dietary sodium is universally connected to blood pressure, but certainly the relationship between levels of sodium in the blood and blood pressure is simple and universal?
The osmotic pressure explanation is what I've always hear as well.
posted by mr_roboto at 7:41 AM on June 23, 2006
I realize there's doubt that dietary sodium is universally connected to blood pressure, but certainly the relationship between levels of sodium in the blood and blood pressure is simple and universal?
The osmotic pressure explanation is what I've always hear as well.
posted by mr_roboto at 7:41 AM on June 23, 2006
The short answer to your question is we don't know for sure.
The data that supports a correlation between high salt diets and hypertension is largely retrospective and population based. There has been no reliable confirmatory prospective studies on the matter to confirm causation. And as far as I know, there is no correlation between serum sodium levels and blood pressure. This link is poorly understood and only presumably causative at this point.
The osmotic explanation is false. In so far as our capillaries are permeable to sodium, sodium doesn't contribute to serum oncotic pressure as it equilibrates between the intra- and extra-vascular space. But this is all beside the point because oncotic pressure and hydrostatic pressure are two different things, and when we measure "blood pressure" we are referring to the latter.
In the case of congestive heart failure, the physiology differs primarily because people with heart failure exhibit a complex dysregulation of salt and fluid balance at the level of the kidney. High salt intake doesn't necessarily exacerbate CHF by causing arterial hypertension; it may do so by worsening fluid retention.
posted by drpynchon at 8:28 AM on June 23, 2006
The data that supports a correlation between high salt diets and hypertension is largely retrospective and population based. There has been no reliable confirmatory prospective studies on the matter to confirm causation. And as far as I know, there is no correlation between serum sodium levels and blood pressure. This link is poorly understood and only presumably causative at this point.
The osmotic explanation is false. In so far as our capillaries are permeable to sodium, sodium doesn't contribute to serum oncotic pressure as it equilibrates between the intra- and extra-vascular space. But this is all beside the point because oncotic pressure and hydrostatic pressure are two different things, and when we measure "blood pressure" we are referring to the latter.
In the case of congestive heart failure, the physiology differs primarily because people with heart failure exhibit a complex dysregulation of salt and fluid balance at the level of the kidney. High salt intake doesn't necessarily exacerbate CHF by causing arterial hypertension; it may do so by worsening fluid retention.
posted by drpynchon at 8:28 AM on June 23, 2006
From what my cardiologist told me, sodium increases fluid retention, which to a certain degree, equals more fluid being pumped around in your veins. More fluid equals higher blood pressure, which means your heart has work harder to pump it.
I do know that, when I eat something salty (I'm on a low sodium diet), I get really thirsty.
posted by doctor_negative at 8:32 AM on June 23, 2006
I do know that, when I eat something salty (I'm on a low sodium diet), I get really thirsty.
posted by doctor_negative at 8:32 AM on June 23, 2006
posted by doctor_negative at 8:40 AM on June 23, 2006
Which comes first, the kidney problem or the heart problem?
This is exactly what's wrong with the organ-oriented model of disease. The kidney works on blood plasma, creating an ultrafiltrate of it to dump out to the bladder and then selectively putting some parts of that ultrafiltrate back in the blood stream. The amount of work the kidney can do is limited by how much blood it receives to work on, and that number is determined by cardiac output, which is related to things like total peripheral resistance of the blood vessels, heart rate, and heart stroke volume.
But the kidney helps the heart out by using endocrine signaling with molecules such as renin in order to help regulate all of the above things. Renin release eventually causes the release of aldosterone from the adrenal glands, and aldosterone instructs the proximal convoluted tubule of the kidney to put filtered sodium back into the bloodstream. Elsewhere in the kidney (I think in the ascending loop of Henle where the aquaporins are?) water "follows" the sodium back into the bloodstream based on a number of factors, one of which is oncotic pressure. The kidney's regulation of this, using urea as a non-ionic solute that won't cross over the membrane, is one of the niftiest and most elegant things in all of biology. The upshot is that maintaining intravascular volume with water is dependent mainly on sodium, and this happens in the kidney.
You have to work really hard to overcome the ability of the heart and kidneys to dump excess dietary sodium. Or, you can be one of those rare people (7% is the number I recall, and most of those African-American) who have some yet-uncharacterized defect that causes them to be less able to dump that excess sodium than the average bear. Maybe it's a defect in signalling set point somewhere in the renin-angiotensin-aldosterone cascade; maybe it's a kidney defect? Who knows.
Now in congestive heart failure (CHF), when the heart isn't able to pump enough blood for the kidney to do its work, the kidney sends a group of signals that amount to a command to increase blood pressure. Sympathetic drive to the heart is increased, but the heart is broken so its rate and stroke volume do not go up. The other way the kidney knows to increase the blood pressure is to retain sodium, thus increasing intravascular volume. The intravascular volume becomes excessive, resulting in a relatively high-pressure but low-flow state; plasma leaks out the capillaries and causes edema (that bloated swelling that folks with CHF get.) It's not healthy, and medical intervention can fix this dysfunctional adaptation.
posted by ikkyu2 at 9:08 AM on June 23, 2006 [1 favorite]
This is exactly what's wrong with the organ-oriented model of disease. The kidney works on blood plasma, creating an ultrafiltrate of it to dump out to the bladder and then selectively putting some parts of that ultrafiltrate back in the blood stream. The amount of work the kidney can do is limited by how much blood it receives to work on, and that number is determined by cardiac output, which is related to things like total peripheral resistance of the blood vessels, heart rate, and heart stroke volume.
But the kidney helps the heart out by using endocrine signaling with molecules such as renin in order to help regulate all of the above things. Renin release eventually causes the release of aldosterone from the adrenal glands, and aldosterone instructs the proximal convoluted tubule of the kidney to put filtered sodium back into the bloodstream. Elsewhere in the kidney (I think in the ascending loop of Henle where the aquaporins are?) water "follows" the sodium back into the bloodstream based on a number of factors, one of which is oncotic pressure. The kidney's regulation of this, using urea as a non-ionic solute that won't cross over the membrane, is one of the niftiest and most elegant things in all of biology. The upshot is that maintaining intravascular volume with water is dependent mainly on sodium, and this happens in the kidney.
You have to work really hard to overcome the ability of the heart and kidneys to dump excess dietary sodium. Or, you can be one of those rare people (7% is the number I recall, and most of those African-American) who have some yet-uncharacterized defect that causes them to be less able to dump that excess sodium than the average bear. Maybe it's a defect in signalling set point somewhere in the renin-angiotensin-aldosterone cascade; maybe it's a kidney defect? Who knows.
Now in congestive heart failure (CHF), when the heart isn't able to pump enough blood for the kidney to do its work, the kidney sends a group of signals that amount to a command to increase blood pressure. Sympathetic drive to the heart is increased, but the heart is broken so its rate and stroke volume do not go up. The other way the kidney knows to increase the blood pressure is to retain sodium, thus increasing intravascular volume. The intravascular volume becomes excessive, resulting in a relatively high-pressure but low-flow state; plasma leaks out the capillaries and causes edema (that bloated swelling that folks with CHF get.) It's not healthy, and medical intervention can fix this dysfunctional adaptation.
posted by ikkyu2 at 9:08 AM on June 23, 2006 [1 favorite]
Thanks ikkyu2, thats very interesting stuff (and hard to find elsewhere). Sorry for the derail thefinned1.
posted by doctor_negative at 9:22 AM on June 23, 2006
posted by doctor_negative at 9:22 AM on June 23, 2006
For 40 years, it was assumed that stomach ulcers were caused by excess secretion of acid in the stomach. Standard treatments included surgery and use of elaborate drugs to try to decrease the amount acid being secreted.
About ten years ago a small group of medical heretics finally managed to create an overwhelming case that most ulcers were actually the result of a bacterial infection, and that the proper way to treat ulcers was with antibiotics. (One of the heretics actually went so far as to drink a solution containing the proposed bacterial agent, and as a result he did develop ulcers which were then successfully treated with antibiotics.)
The point being that medical science is not as advanced as some people believe. Not everything they declare is actually a fact.
posted by Steven C. Den Beste at 9:29 AM on June 23, 2006
About ten years ago a small group of medical heretics finally managed to create an overwhelming case that most ulcers were actually the result of a bacterial infection, and that the proper way to treat ulcers was with antibiotics. (One of the heretics actually went so far as to drink a solution containing the proposed bacterial agent, and as a result he did develop ulcers which were then successfully treated with antibiotics.)
The point being that medical science is not as advanced as some people believe. Not everything they declare is actually a fact.
posted by Steven C. Den Beste at 9:29 AM on June 23, 2006
Which comes first, the kidney problem or the heart problem?
It depends. Kidney disease can cause heart failure. Heart failure can cause kidney disease. And both can be caused by neuroendocrine/hormonal dysfunction. In the case of viral cardiomyopathies (as your doctor is suggesting) the primary insult is most likely to the heart.
As ikkyu2 notes, the way the body maintains homeostasis with respect to blood pressure, fluid status, and electrolytes involves a very complex interplay of multiple organ systems, reflex circuits, and circulating chemical messengers and effectors.
posted by drpynchon at 11:01 AM on June 23, 2006
It depends. Kidney disease can cause heart failure. Heart failure can cause kidney disease. And both can be caused by neuroendocrine/hormonal dysfunction. In the case of viral cardiomyopathies (as your doctor is suggesting) the primary insult is most likely to the heart.
As ikkyu2 notes, the way the body maintains homeostasis with respect to blood pressure, fluid status, and electrolytes involves a very complex interplay of multiple organ systems, reflex circuits, and circulating chemical messengers and effectors.
posted by drpynchon at 11:01 AM on June 23, 2006
My comment above is an attempt to summarize something that took me a long time to learn about; I found the topic so fascinating that I studied it in great detail, far greater than I ever need to use in my working life.
Anyone with a college-level grasp of chemistry and quantitative reasoning could read the peerless Burton David Rose's Clinical Physiology of Acid-Base and Electrolyte Disorders to learn everything they ever wanted to know about this topic. In fact, I see it's out in a new edition; I'm sorely tempted myself.
As Steven Den Beste points out, we're still learning about this. One of the interesting things about the model of CHF I outlined is that it relates everything to a weak pump. You would expect, based on this model, that giving someone a drug that increased the power of the pump would help to fix the problem, increasing health. So for many years this was done - people took isoproteronol and other drugs, beta agonists, drugs that mimic adrenaline and increase the pumping power of the heart.
Then someone thought to study the effect of this treatment in an outcome-based, controlled, blinded way. Turns out that, in the setting of CHF, these drugs increased mortality; people who took 'em had more heart attacks and died sooner. Thousands probably died early from this misguided attempt to help.
Based on this, someone else thought to try beta blockers in CHF. Beta blockers interfere with the effects of natural adrenaline on the heart, causing the heart to beat slower and more weakly. You would think that if the problem was a weak pump, a medicine that weakens the pump output still further wouldn't help. But in fact people with CHF on beta blockers have fewer heart attacks and live longer than they otherwise would!
Medical science isn't as advanced as some people believe, but to me at least it appears that we're making strong headway; we've learned so much in the last 50 years that it boggles the intelligent mind.
posted by ikkyu2 at 3:26 PM on June 23, 2006
Anyone with a college-level grasp of chemistry and quantitative reasoning could read the peerless Burton David Rose's Clinical Physiology of Acid-Base and Electrolyte Disorders to learn everything they ever wanted to know about this topic. In fact, I see it's out in a new edition; I'm sorely tempted myself.
As Steven Den Beste points out, we're still learning about this. One of the interesting things about the model of CHF I outlined is that it relates everything to a weak pump. You would expect, based on this model, that giving someone a drug that increased the power of the pump would help to fix the problem, increasing health. So for many years this was done - people took isoproteronol and other drugs, beta agonists, drugs that mimic adrenaline and increase the pumping power of the heart.
Then someone thought to study the effect of this treatment in an outcome-based, controlled, blinded way. Turns out that, in the setting of CHF, these drugs increased mortality; people who took 'em had more heart attacks and died sooner. Thousands probably died early from this misguided attempt to help.
Based on this, someone else thought to try beta blockers in CHF. Beta blockers interfere with the effects of natural adrenaline on the heart, causing the heart to beat slower and more weakly. You would think that if the problem was a weak pump, a medicine that weakens the pump output still further wouldn't help. But in fact people with CHF on beta blockers have fewer heart attacks and live longer than they otherwise would!
Medical science isn't as advanced as some people believe, but to me at least it appears that we're making strong headway; we've learned so much in the last 50 years that it boggles the intelligent mind.
posted by ikkyu2 at 3:26 PM on June 23, 2006
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The best illustration of this was when treatment for congestive heart failure wasn't so great, just ten years ago or so, and the ED would fill up with people in acute distress with fluid on their lungs after the Super Bowl from eating too many salty snacks.
posted by docpops at 6:50 AM on June 23, 2006