How Big is Your Brain (Natriuretic Peptide)?

While shadowing some all-star PAs in the ER, I’ve heard the term/lab value BNP mentioned often in relation to heart failure patients. Let’s see what BNP is all about.

BNP stands for “Brain Natriuretic Peptide” or B-type natriuretic peptide and is also called ventricular natriuretic peptide. What a mouthful. It’s a biochemical marker that can help diagnose heart failure and is measured via the serum or plasma of our blood.

In terms of anatomy and physiology which I’m currently studying, BNP is first mentioned in the endocrine chapter as one of two hormones secreted by cardiac cells (the other is ANP, which stands for atrial natriuretic peptide). Now I know what you’re thinking, if these are both secreted by cardiac cells, why on earth is BNP called “brain natriuretic peptide.” Because… reasons: it was initially found in brain tissue of pigs and the name stuck. 

ANP is secreted by cells in the wall of the right atrium, and BNP the ventricles (mainly the left). ANP responds to blood volume and pressure and BNP responds to stretching/tension.

The word natrium (Latin) refers to sodium, -ouresis means urination, and peptide is a protein. This hints that BNP probably increases the expelling of salt in our urine, meaning a fluid loss, meaning an eventual blood volume loss and loss in blood pressure. Natriuresis literally means the excretion of salt in the urine. What triggers the release of BNP is the abnormal stretching of the heart walls. So if our heart is being stretched abnormally, something is wrong, right? Either there is too much pressure or blood, or the heart is weakened and not pumping blood effectively, which is where heart failure comes in. And if the heart is weakened, then pressure and volume will increase as it struggles to keep up. Makes sense.

Remember that heart failure can cause respiratory symptoms, distress even. If there is a problem with the heart, then either too much or not enough blood is going to enter the lungs. If there’s not enough, then proper gas exchange isn’t going to occur and our body will be starved of oxygen, causing us to breathe faster. Fluid build up can also enter the alveoli causing respiratory problems.

Effects

We learn more about ANP and BNP in the blood vessels and circulation chapter of A&P where we learn their effects:

  1. Increase sodium ion excretion by the kidneys. 

  2. Promote water loss by increasing urine volume.

  3. Reduce thirst.

  4. Block the release of ADH, aldosterone, epinephrine, and norepinephrine.

  5. Stimulate peripheral vasodilation.

Yea, so they don’t mess around. Once these five things reduce blood volume and pressure (therefore restoring homeostasis), the natriuretic peptides stop being excreted by our cardiac cells because they’ve done their job. That’s a negative feedback loop.

Let’s talk a little bit about #4 because we just mentioned four other hormones. 

  • ADH, the antidiuretic hormone, is secreted by the posterior pituitary (which also secretes oxytocin). Its function is in its name; it prevents uresis, or urination. In other words, it retains fluids. This is the hormone inhibited by alcohol, which is why we urinate when we imbibe. BNP does the same thing (except for making us drunk); it makes us urinate. BNP is blocking the release of ADH.

  • Aldosterone is secreted by the adrenal cortex of the adrenal gland. I like to think that it keeps “al dos” salts. And salt retention = fluid retention. Aldosterone is involved in the renin-angiotensin-aldosterone system (RAAS). BNP is blocking the release of aldosterone.

  • So what about epinephrine and norepinephrine? Well norepinephrine and epinephrine are vasopressors, which raise blood pressure. BNP is blocking those too.

Heart Failure & Shortness of Breath

When I was studying for the NREMT, I made the following note about heart failure:

LEFT-SIDED HEART FAILURE is associated with pulmonary edema and leads to shortness of breath because as blood is returning via the pulmonary veins to the left atrium and then left ventricle, the ventricle can’t pump out as much and there is fluid build-up in the lungs. Pink and frothy sputum found here. THINK L AND LEFT FOR LUNGS AND LYING DOWN! You will see respiratory issues like shortness of breath. The patient worsens when they lie down and worsens when they exert themselves because they can’t breathe adequately.

“An accurate and rapid diagnosis is crucial for the diagnosis of patients who present to the emergency room or outpatient examination room with acute respiratory distress.” (Yoo, 2014). So respiratory distress is a major symptom of heart failure. There we go.

Questions

  1. What about other sources of high blood pressure? Wouldn’t that trigger BNP? Can’t you have HBP but not heart failure?

  2. Aren’t BNPs block of epinephrine and norepinephrine counterproductive towards making the heart stronger? Don’t these make the heart, that is already struggling, weaker?

  3. If BNP is a protein and water-soluble, can it be detected in the urine?

    The data suggest that urine BNP is a new candidate marker for diagnosis and prognosis of HF mortality and cardiac events. This raises the possibility of using this relatively simple noninvasive test in primary care settings or in specific conditions where the collection of blood samples could be difficult. Source.

  4. Could high salt levels in the urine also point to heart failure?

Sources

Cortés R, Rivera M, Salvador A, García de Burgos F, Bertomeu V, Roselló-Lletí E, Martínez-Dolz L, Payá R, Almenar L, Portolés M. Urinary B-type natriuretic peptide levels in the diagnosis and prognosis of heart failure. J Card Fail. 2007 Sep;13(7):549-55. doi: 10.1016/j.cardfail.2007.04.007. PMID: 17826645. https://pubmed.ncbi.nlm.nih.gov/17826645/

Martini F, Nath J, Bartholomew E. Fundamentals of Anatomy & Physiology. 2018. Eleventh Edition. Pearson Education. 

Yoo BS. Clinical Significance of B-type Natriuretic Peptide in Heart Failure. J Lifestyle Med. 2014;4(1):34-38. doi:10.15280/jlm.2014.4.1.34 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4390764/